Displaying publications 1 - 20 of 1079 in total

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  1. Fulltext A Bottom-Up Synthesis Approach to Silver Nanoparticles Induces Anti-Proliferative and Apoptotic Activities Against MCF-7, MCF-7/TAMR-1 and MCF-10A Human Breast Cell Lines
    Zulkifli NI, Muhamad M, Mohamad Zain NN, Tan WN, Yahaya N, Bustami Y, et al.
    Molecules, 2020 Sep 22;25(18).
    PMID: 32971740 DOI: 10.3390/molecules25184332
    A bottom-up approach for synthesizing silver nanoparticles (AgNPs-GA) phytomediated by Garcinia atroviridis leaf extract is described. Under optimized conditions, the AgNPs-GA were synthesized at a concentration of 0.1 M silver salt and 10% (w/v) leaf extract, 1:4 mixing ratio of reactants, pH 3, temperature 32 °C and 72 h reaction time. The AgNPs-GA were characterized by various analytical techniques and their size was determined to be 5-30 nm. FTIR spectroscopy indicates the role of phenolic functional groups in the reduction of silver ions into AgNPs-GA and in supporting their subsequent stability. The UV-Visible spectrum showed an absorption peak at 450 nm which reflects the surface plasmon resonance (SPR) of AgNPs-GA and further supports the stability of these biosynthesized nanoparticles. SEM, TEM and XRD diffractogram analyses indicate that AgNPs-GA were spherical and face-centered-cubic in shape. This study also describes the efficacy of biosynthesized AgNPs-GA as anti-proliferative agent against human breast cancer cell lines, MCF-7 and MCF-7/TAMR-1. Our findings indicate that AgNPs-GA possess significant anti-proliferative effects against both the MCF-7 and MCF-7/TAMR-1 cell lines, with inhibitory concentration at 50% (IC50 values) of 2.0 and 34.0 µg/mL, respectively, after 72 h of treatment. An induction of apoptosis was evidenced by flow cytometry using Annexin V-FITC and propidium iodide staining. Therefore, AgNPs-GA exhibited its anti-proliferative activity via apoptosis on MCF-7 and MCF-7/TAMR-1 breast cancer cells in vitro. Taken together, the leaf extract from Garcinia atroviridis was found to be highly capable of producing AgNPs-GA with favourable physicochemical and biological properties.
    Matched MeSH terms: Cell Proliferation/drug effects
  2. Improved cellular response of chemically crosslinked collagen incorporated hydroxyethyl cellulose/poly(vinyl) alcohol nanofibers scaffold
    Zulkifli FH, Jahir Hussain FS, Abdull Rasad MS, Mohd Yusoff M
    J Biomater Appl, 2015 Feb;29(7):1014-27.
    PMID: 25186524 DOI: 10.1177/0885328214549818
    The aim of this research is to develop biocompatible nanofibrous mats using hydroxyethyl cellulose with improved cellular adhesion profiles and stability and use these fibrous mats as potential scaffold for skin tissue engineering. Glutaraldehyde was used to treat the scaffolds water insoluble as well as improve their biostability for possible use in biomedical applications. Electrospinning of hydroxyethyl cellulose (5 wt%) with poly(vinyl alcohol) (15 wt%) incorporated with and without collagen was blended at (1:1:1) and (1:1) ratios, respectively, and was evaluated for optimal criteria as tissue engineering scaffolds. The nanofibrous mats were crosslinked and characterized by scanning electron microscope, Fourier transform infrared spectroscopy, differential scanning calorimetry, and thermogravimetric analysis. Scanning electron microscope images showed that the mean diameters of blend nanofibers were gradually increased after chemically crosslinking with glutaraldehyde. Fourier transform infrared spectroscopy was carried out to understand chemical interactions in the presence of aldehyde groups. Thermal characterization results showed that the stability of hydroxyethyl cellulose/poly(vinyl alcohol) and hydroxyethyl cellulose/poly(vinyl alcohol)/collagen nanofibers was increased with glutaraldehyde treatment. Studies on cell-scaffolds interaction were carried out by culturing human fibroblast (hFOB) cells on the nanofibers by assessing the growth, proliferation, and morphologies of cells. The scanning electron microscope results show that better cell proliferation and attachment appeared on hydroxyethyl cellulose/poly(vinyl alcohol)/collagen substrates after 7 days of culturing, thus, promoting the potential of electrospun scaffolds as a promising candidate for tissue engineering applications.
    Matched MeSH terms: Cell Proliferation
  3. Nanostructured materials from hydroxyethyl cellulose for skin tissue engineering
    Zulkifli FH, Hussain FSJ, Rasad MSBA, Mohd Yusoff M
    Carbohydr Polym, 2014 Dec 19;114:238-245.
    PMID: 25263887 DOI: 10.1016/j.carbpol.2014.08.019
    In this study, a novel fibrous membrane of hydroxyethyl cellulose (HEC)/poly(vinyl alcohol) blend was successfully fabricated by electrospinning technique and characterized. The concentration of HEC (5%) with PVA (15%) was optimized, blended in different ratios (30-50%) and electrospun to get smooth nanofibers. Nanofibrous membranes were made water insoluble by chemically cross-linking by glutaraldehyde and used as scaffolds for the skin tissue engineering. The microstructure, morphology, mechanical and thermal properties of the blended HEC/PVA nanofibrous scaffolds were characterized by scanning electron microscope, Fourier transform infrared spectroscopy, differential scanning colorimetry, universal testing machine and thermogravimetric analysis. Cytotoxicity studies on these nanofibrous scaffolds were carried out using human melanoma cells by the MTT assays. The cells were able to attach and spread in the nanofibrous scaffolds as shown by the SEM images. These preliminary results show that these nanofibrous scaffolds that supports cell adhesion and proliferation is promising for skin tissue engineering.
    Matched MeSH terms: Cell Proliferation/physiology
  4. Cytotoxicity evaluation of ketoprofen found in pharmaceutical wastewater on HEK 293 cell growth and metabolism
    Zulkarnain NN, Anuar N, Johari NA, Sheikh Abdullah SR, Othman AR
    Environ Toxicol Pharmacol, 2020 Nov;80:103498.
    PMID: 32950717 DOI: 10.1016/j.etap.2020.103498
    Inefficient ketoprofen removal from pharmaceutical wastewater may negatively impact the ecosystem and cause detrimental risks to human health. This study was conducted to determine the cytotoxicity effects of ketoprofen on HEK 293 cell growth and metabolism, including cyclooxygenase-1 (COX-1) expression, at environmentally relevant concentrations. The cytotoxic effects were evaluated through the trypan blue test, DNS assay, MTT assay, and the expression ratio of the COX-1 gene. The results of this study show insignificant (p > 0.05) cytotoxic effects of ketoprofen on cell viability and cell metabolism. However, high glucose consumption rates among the treated cells cause an imitation of the Warburg effect, which is likely linked to the development of cancer cells. Apart from that, the upregulation of COX-1 expression among the treated cells indicates remote possibility of inflammation. Although no significant cytotoxic effects of ketoprofen were detected throughout this study, the effects of prolonged exposure of residual ketoprofen need to be evaluated in the future.
    Matched MeSH terms: Cell Proliferation/drug effects
  5. Fulltext Extreme Thrombocytosis in a Child: Laboratory Approaches and Diagnostic Challenges
    Zulkafli Z, Janaveloo T, Wan Ab Rahman WS, Hassan MN, Abdullah WZ
    Oman Med J, 2019 Jul;34(4):336-340.
    PMID: 31360323 DOI: 10.5001/omj.2019.65
    Thrombocytosis in children as well as in adult is defined as platelet count ≥ 450 × 109/L, and it is usually a reactive feature to various medical disorders. However, extreme thrombocytosis (platelet count ≥ 1000 × 109/L) is an uncommon finding among pediatric and adult patients, which may indicate more than a reactive phenomenon. We describe a case of a five-year-old boy who was admitted due to recurrent epistaxis. He had no history of allergic tendency or trauma. Physical examination was unremarkable except for shotty neck nodes. Laboratory results at presentation showed normal hemoglobin and total leukocyte count with eosinophilia (0.92 × 109/L), and extreme thrombocytosis. Other relevant investigations including coagulation profile, serum ferritin, liver, and renal function tests were all within normal ranges. Stool samples for ova and cysts were negative. The peripheral blood smear and bone marrow aspirate confirmed thrombocytosis with increased megakaryocytic proliferation and no artefactual reasons for the high platelets such as red blood cell fragments. Different causes of thrombocytosis in childhood were investigated after considering the possible differential diagnoses for extreme thrombocytosis.
    Matched MeSH terms: Cell Proliferation
  6. Fulltext In vivo response of GsdmA3(Dfl)/+ mice to topically applied fish oil - effects on cellular markers and macrophages
    Zulfakar MH, Porter RM, Heard CM
    FEBS Open Bio, 2016 08;6(8):827-34.
    PMID: 27516961 DOI: 10.1002/2211-5463.12095
    Psoriasis is an incurable autoimmune disease characterized by patches of abnormal red, itchy and scaly skin. This work examined the modulation of inflammation, hyperproliferation and immune cell markers following topical application of fish oil (FO) in comparison to the antipsoriatic agents, betamethasone dipropionate (BD) and salicylic acid (SA), to GsdmA3(Dfl)/+ mice, a hair loss mutant which also exhibits epidermal hyperproliferation akin to psoriasis. The mice were dosed with 100 mg of the test formulation and after 10 days, the mice were sacrificed, skin sections excised and subjected to immunohistochemical determination of COX-2, K17 and MAC-1; and immunofluorescence of Ki-67. Unchanged expression of the proinflammatory enzyme COX-2 was observed in all treatments, suggesting the noninvolvement of COX-2 in the aetiology of cutaneous aberration seen in GsdmA3(Dfl)/+ mice. Intense staining of K17 and MAC-1 in the FO-treated group mirrored the epidermal thickening seen observed in live mice by optical coherence tomography (OCT). The ratio of Ki-67-positive nuclei per 100 basal cells indicated that hyperproliferation of keratinocytes occurred in FO-treated mice and the opposite was true for BD-treated mice. There was a positive correlation (R (2) 0.995) between Ki-67 and the epidermal thickness data observed previously. In all immunochemical procedures, the combined BD, SA and FO formulation did not show any significant difference with the control group, reflecting observations seen previously. In conclusion, the epidermal changes observed following topical FO treatment on GsdmA3(Dfl)/+ mice involves an increase in cellular proliferation and macrophages, although COX-2 does not appear to play an important role.
    Matched MeSH terms: Cell Proliferation
  7. Fulltext Mobility-Enhanced Reliable Geographical Forwarding in Cognitive Radio Sensor Networks
    Zubair S, Syed Yusoff SK, Fisal N
    Sensors (Basel), 2016;16(2):172.
    PMID: 26840312 DOI: 10.3390/s16020172
    The emergence of the Internet of Things and the proliferation of mobile wireless devices has brought the area of mobile cognitive radio sensor networks (MCRSN) to the research spot light. Notwithstanding the potentials of CRSNs in terms of opportunistic channel usage for bursty traffic, the effect of the mobility of resource-constrained nodes to route stability, mobility-induced spatio-temporal spectral opportunities and primary user (PU) protection still remain open issues that need to be jointly addressed. To this effect, this paper proposes a mobile reliable geographical forwarding routing (MROR) protocol. MROR provides a robust mobile framework for geographical forwarding that is based on a mobility-induced channel availability model. It presents a comprehensive routing strategy that considers PU activity (to take care of routes that have to be built through PU coverage), PU signal protection (by the introduction of a mobility-induced guard (mguard) distance) and the random mobility-induced spatio-temporal spectrum opportunities (for enhancement of throughput). It also addresses the issue of frequent route maintenance that arises when speeds of the mobile nodes are considered as a routing metric. As a result, simulation has shown the ability of MROR to reduce the route failure rate by about 65% as against other schemes. In addition, further results show that MROR can improve both the throughput and goodput at the sink in an energy-efficient manner that is required in CRSNs as against compared works.
    Matched MeSH terms: Cell Proliferation
  8. Annona muricata leaves induce G₁ cell cycle arrest and apoptosis through mitochondria-mediated pathway in human HCT-116 and HT-29 colon cancer cells
    Zorofchian Moghadamtousi S, Karimian H, Rouhollahi E, Paydar M, Fadaeinasab M, Abdul Kadir H
    J Ethnopharmacol, 2014 Oct 28;156:277-89.
    PMID: 25195082 DOI: 10.1016/j.jep.2014.08.011
    ETHNOPHARMACOLOGICAL RELEVANCE: Annona muricata known as "the cancer killer" has been widely used in the traditional medicine for the treatment of cancer and tumors. The purpose of this study is to investigate the anticancer properties of ethyl acetate extract of Annona muricata leaves (EEAM) on HT-29 and HCT-116 colon cancer cells and the underlying mechanisms.
    MATERIALS AND METHODS: The effect of EEAM on the cell proliferation of HT-29 and HCT-116 cells was analyzed by the MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium) assay. High content screening system (HCS) was applied to investigate the cell membrane permeability, mitochondrial membrane potential (MMP), nuclear condensation and cytochrome c translocation from mitochondria to cytosol. Reactive oxygen species (ROS) formation, lactate dehydrogenase (LDH) release and activation of caspase-3/7, -8 and -9 were measured while treatment. Flow cytometric analysis was used to determine the cell cycle distribution and phosphatidylserine externalization. The protein expression of Bax and Bcl-2 was determined using immunofluorescence analysis. In addition, the potential of EEAM to suppress the migration and invasion of colon cancer cells was also examined.
    RESULTS: EEAM exerted significant cytotoxic effects on HCT-116 and HT-29 cells as determined by MTT and LDH assays. After 24 h treatment, EEAM exhibited the IC₅₀ value of 11.43 ± 1.87 µg/ml and 8.98 ± 1.24 µg/ml against HT-29 and HCT-116 cells, respectively. Flow cytometric analysis demonstrated the cell cycle arrest at G1 phase and phosphatidylserine externalization confirming the induction of apoptosis. EEAM treatment caused excessive accumulation of ROS followed by disruption of MMP, cytochrome c leakage and activation of the initiator and executioner caspases in both colon cancer cells. Immunofluorescence analysis depicted the up-regulation of Bax and down-regulation of Bcl-2 proteins while treated with EEAM. Furthermore, EEAM conspicuously blocked the migration and invasion of HT-29 and HCT-116 cells.
    CONCLUSIONS: These findings provide a scientific basis for the use of A. muricata leaves in the treatment of cancer, although further in vivo studies are still required.
    Matched MeSH terms: Cell Proliferation/drug effects
  9. Fulltext The chemopotential effect of Annona muricata leaves against azoxymethane-induced colonic aberrant crypt foci in rats and the apoptotic effect of Acetogenin Annomuricin E in HT-29 cells: a bioassay-guided approach
    Zorofchian Moghadamtousi S, Rouhollahi E, Karimian H, Fadaeinasab M, Firoozinia M, Ameen Abdulla M, et al.
    PLoS One, 2015;10(4):e0122288.
    PMID: 25860620 DOI: 10.1371/journal.pone.0122288
    Annona muricata has been used in folk medicine for the treatment of cancer and tumors. This study evaluated the chemopreventive properties of an ethyl acetate extract of A. muricata leaves (EEAML) on azoxymethane-induced colonic aberrant crypt foci (ACF) in rats. Moreover, the cytotoxic compound of EEAML (Annomuricin E) was isolated, and its apoptosis-inducing effect was investigated against HT-29 colon cancer cell line using a bioassay-guided approach. This experiment was performed on five groups of rats: negative control, cancer control, EEAML (250 mg/kg), EEAML (500 mg/kg) and positive control (5-fluorouracil). Methylene blue staining of colorectal specimens showed that application of EEAML at both doses significantly reduced the colonic ACF formation compared with the cancer control group. Immunohistochemistry analysis showed the down-regulation of PCNA and Bcl-2 proteins and the up-regulation of Bax protein after administration of EEAML compared with the cancer control group. In addition, an increase in the levels of enzymatic antioxidants and a decrease in the malondialdehyde level of the colon tissue homogenates were observed, suggesting the suppression of lipid peroxidation. Annomuricin E inhibited the growth of HT-29 cells with an IC50 value of 1.62 ± 0.24 μg/ml after 48 h. The cytotoxic effect of annomuricin E was further substantiated by G1 cell cycle arrest and early apoptosis induction in HT-29 cells. Annomuricin E triggered mitochondria-initiated events, including the dissipation of the mitochondrial membrane potential and the leakage of cytochrome c from the mitochondria. Prior to these events, annomuricin E activated caspase 3/7 and caspase 9. Upstream, annomuricin E induced a time-dependent upregulation of Bax and downregulation of Bcl-2 at the mRNA and protein levels. In conclusion, these findings substantiate the usage of A. muricata leaves in ethnomedicine against cancer and highlight annomuricin E as one of the contributing compounds in the anticancer activity of A. muricata leaves.
    Matched MeSH terms: Cell Proliferation/drug effects
  10. Sea cucumber (Stichopus hermanii) based hydrogel to treat burn wounds in rats
    Zohdi RM, Zakaria ZA, Yusof N, Mustapha NM, Abdullah MN
    J Biomed Mater Res B Appl Biomater, 2011 Jul;98(1):30-7.
    PMID: 21504052 DOI: 10.1002/jbm.b.31828
    Malaysian sea cucumber was incorporated into hydrogel formulation by using electron beam irradiation technique and was introduced as novel cross-linked Gamat Hydrogel dressing. This study investigated whether Gamat Hydrogel enhanced repair of deep partial skin thickness burn wound in rats and its possible mechanism. Wounds were treated with either Gamat Hydrogel, control hydrogel, OpSite® film dressing or left untreated. Skin samples were taken at 7, 14, 21, and 28 days post burn for histological and molecular evaluations. Gamat Hydrogel markedly enhanced wound contraction and improved histological reorganization of the regenerating tissue. Furthermore, the dressing modulated the inflammatory responses, stimulated the activation and proliferation of fibroblasts, and enhanced rapid production of collagen fiber network with a consequently shorter healing time. The level of proinflammatory cytokines; IL-1α, IL-1β, and IL-6, were significantly reduced in Gamat Hydrogel treated wounds compared with other groups as assessed by reverse transcription-polymerase chain reaction (RT-PCR). In summary, our results showed that Gamat Hydrogel promoted burn wound repair via a complex mechanism involving stimulation of tissue regeneration and regulation of pro-inflammatory cytokines. The resultant wound healing effects were attributed to the synergistic effect of the hydrogel matrix and incorporated sea cucumber.
    Matched MeSH terms: Cell Proliferation/drug effects
  11. Fulltext Regulation of Hippo/YAP signaling and Esophageal Squamous Carcinoma progression by an E3 ubiquitin ligase PARK2
    Zhou X, Li Y, Wang W, Wang S, Hou J, Zhang A, et al.
    Theranostics, 2020;10(21):9443-9457.
    PMID: 32863938 DOI: 10.7150/thno.46078
    Objective: Esophageal squamous cell carcinoma (ESCC) is one of the most commonly diagnosed cancer types in China. Recent genomic sequencing analysis indicated the over-activation of Hippo/YAP signaling might play important roles for the carcinogenic process and progression for ESCC patients. However, little is known about the molecular mechanisms that controls Hippo signaling activity in ESCC. Our previous studies indicated that PLCE1-an important risk factor for ESCC-linked to ESCC progression through snail signaling, during this period, we found PARK2 was an important downstream target of PLCE1-snail axis. PARK2 was decreased in ESCC human samples, and correlated with good prognosis in ESCC patients. Further research showed that PARK2 could inhibit YAP, which functions as key downstream effectors of the Hippo pathway. Here, we aim to reveal the molecular mechanisms of PARK2 modulated Hippo pathway in ESCC. Methods: To evaluate the function of PARK2 in ESCC, we used a tissue microarray (TMA) of 223 human ESCC patients and immunohistochemistry to analyze the correlation between PARK2 expression and clinicopathologic variables. Depletion of endogenous PARK2 and YAP from ESCC cells using CRISPR/Cas9 technologies. Flow cytometry and EdU cell proliferation assay were used to detect proliferation of ESCC cells. Nude mice subcutaneous injection and Ki-67 staining were used to evaluate tumor growth in vivo. Migration and invasion assays were performed. In addition, lung metastasis models in mice were used to validate the function of PARK2 in vivo. Identification of PARK2 involved in hippo pathway was achieved by expression microarray screening, double immunofluorescence staining and co-immunoprecipitation assays. The RNA-seq analysis results were validated through quantitative real-time PCR (qRT-PCR) analysis. The protein half-life of YAP was analyzed by Cycloheximide assay, and the TEAD activity was detected by Luciferase reporter assays. Results: Clinical sample of ESCC revealed that low PARK2 expression correlated with late tumor stage (P < 0.001), poor differentiation (P < 0.04), lymph node (P < 0.001) and distant metastasis (P = 0.0087). Multivariate Cox proportional regression analysis further revealed that PARK2 expression (P = 0.032) is an independent prognostic factor for the overall survival of ESCC patients. Besides, the immunohistochemistry results showed that PARK2 negatively correlated with YAP protein level (P < 0.001). PARK2 depletion promotes ESCC progression both through Hippo/YAP axis, while PARK2 overexpression suppresses ESCC tumor progression by Hippo signaling. Co-IP and ubiquitination assays revealed that PARK2 could interact with YAP in the cytosol and promotes YAP K48-linked ubiquitination at K90 sites. Conclusion: Clinical sample analysis and mechanistic study have validated PARK2 as a tumor suppressor for ESCC. Multivariate Cox proportional regression analysis further revealed that PARK2 is an independent prognostic factor for the overall survival of ESCC patients. Cellular and molecular mechanisms in this study showed that PARK2 associated with YAP protein in the cytosol, promoted YAP ubiquitination and proteasome-dependent degradation in ESCC cells. Therefore, as a novel modulator for Hippo signaling, modulation of PARK2 activity or gene expression level could be an appealing strategy to treat esophageal.
    Matched MeSH terms: Cell Proliferation/genetics
  12. Fulltext Extract from the paralyzed spinal cord of rats enhances neural stem cell proliferation in the neonatal rat brain by upregulating the Notch1/Hes1 pathway
    Zhou Q, Tian L, Jia X, Ling KH, Mohd Nor NH, Harun MH, et al.
    Minerva Pediatr (Torino), 2023 Oct;75(5):780-783.
    PMID: 37284814 DOI: 10.23736/S2724-5276.23.07322-6
    Matched MeSH terms: Cell Proliferation
  13. MenSCs Transplantation Improve the Viability of Injured Endometrial Cells Through Activating PI3K/Akt Pathway
    Zhang S, Zhang R, Yin X, Lu Y, Cheng H, Pan Y, et al.
    Reprod Sci, 2023 Nov;30(11):3325-3338.
    PMID: 37308799 DOI: 10.1007/s43032-023-01282-0
    Endometrial injury is one of the leading causes of female infertility and is caused by intrauterine surgery, endometrial infection, repeated abortion, or genital tuberculosis. Currently, there is little effective treatment to restore the fertility of patients with severe intrauterine adhesions and thin endometrium. Recent studies have confirmed the promising therapeutic effects of mesenchymal stem cell transplantation on various diseases with definite tissue injury. The aim of this study is to investigate the improvements of menstrual blood-derived endometrial stem cells (MenSCs) transplantation on functional restoration in the endometrium of mouse model. Therefore, ethanol-induced endometrial injury mouse models were randomly divided into two groups: the PBS-treated group, and the MenSCs-treated group. As expected, the endometrial thickness and gland number in the endometrium of MenSCs-treated mice were significantly improved compared to those of PBS-treated mice (P cells, which is likely contributed by activating the PI3K/Akt signaling pathway. Further tests also confirmed the chemotaxis of GFP-labeled MenSCs towards the injured uterus. Consequently, MenSCs treatment significantly improved the pregnant mice and the number of embryos in pregnant mice. This study confirmed the superior improvements of MenSCs transplantation on the injured endometrium and uncovered the potential therapeutic mechanism, which provides a promising alternative for patients with serious endometrial injury.
    Matched MeSH terms: Cell Proliferation/physiology
  14. Fulltext 10H-3,6-Diazaphenothiazine induces G2/M phase cell cycle arrest and caspase-dependent apoptosis and inhibits cell invasion of A2780 ovarian carcinoma cells through the regulation of NF-κB and (BIRC6-XIAP) complexes
    Zhang J, Ming C, Zhang W, Okechukwu PN, Morak-Młodawska B, Pluta K, et al.
    Drug Des Devel Ther, 2017;11:3045-3063.
    PMID: 29123378 DOI: 10.2147/DDDT.S144415
    The asymptomatic properties and high treatment resistance of ovarian cancer result in poor treatment outcomes and high mortality rates. Although the fundamental chemotherapy provides promising anticancer activities, it is associated with severe side effects. The derivative of phenothiazine, namely, 10H-3,6-diazaphenothiazine (PTZ), was synthesized and reported with ideal anticancer effects in a previous paper. In this study, detailed anticancer properties of PTZ was examined on A2780 ovarian cancer cells by investigating the cytotoxicity profiles, mechanism of apoptosis, and cell invasion. Research outcomes revealed PTZ-induced dose-dependent inhibition on A2780 cancer cells (IC50 =0.62 µM), with significant less cytotoxicity toward HEK293 normal kidney cells and H9C2 normal heart cells. Generation of reactive oxygen species (ROS) and polarization of mitochondrial membrane potential (ΔΨm) suggests PTZ-induced cell death through oxidative damage. The RT2 Profiler PCR Array on apoptosis pathway demonstrated PTZ-induced apoptosis via intrinsic (mitochondria-dependent) and extrinsic (cell death receptor-dependent) pathway. Inhibition of NF-κB and subsequent inhibition of (BIRC6-XIAP) complex activities reduced the invasion rate of A2780 cancer cells penetrating through the Matrigel™ Invasion Chamber. Lastly, the cell cycle analysis hypothesizes that the compound is cytostatic and significantly arrests cell proliferation at G2/M phase. Hence, the exploration of the underlying anticancer mechanism of PTZ suggested its usage as promising chemotherapeutic agent.
    Matched MeSH terms: Cell Proliferation/drug effects
  15. TEOA, a triterpenoid from Actinidia eriantha, induces autophagy in SW620 cells via endoplasmic reticulum stress and ROS-dependent mitophagy
    Zhang D, Gao C, Li R, Zhang L, Tian J
    Arch Pharm Res, 2017 May;40(5):579-591.
    PMID: 28211011 DOI: 10.1007/s12272-017-0899-9
    2α,3α,24-Thrihydroxyurs-12-en-28-oicacid (TEOA), a pentacyclic triterpenoid, isolated from the roots of Actinidia eriantha, exhibits significant cytotoxicity against SW620, BGC-823, HepG-2, A549 and PC-3 cancer cells. In this study, we investigated the underlying molecular mechanism of the anticancer activity of TEOA in SW620 cells. We demonstrated that TEOA induced apoptosis through cleavage of caspase-9 and PARP in SW620 cells. In addition, evidence of TEOA-mediated autophagy included the induction of autophagolysosomes and activation of autophagic markers LC-3B and p62. Further analysis illustrated that TEOA promoted the phosphorylation of PERK and elF2α, followed by up-regulation of the downstream protein CHOP, suggesting the involvement of PERK/eIF2α/CHOP pathway and ER stress in TEOA-induced autophagy in SW620 cells. Meanwhile, TEOA-mediated PINK1, Parkin, ubiquitin and p62 activation revealed that TEOA induced specific autophagy-mitophagy in SW620 cells. Additionally, an antioxidant NAC attenuated the TEOA-induced mitophagy, indicating that TEOA triggers mitophagy via a ROS-dependent pathway. Collectively, our findings revealed a novel cellular mechanism of TEOA in the colon cancer cell line SW620, thus providing a molecular basis for developing TEOA into an anti-tumor candidate.
    Matched MeSH terms: Cell Proliferation/drug effects
  16. MiR-26b-3p Promotes Intestinal Motility Disorder by Targeting FZD10 to Inhibit GSK3β/β-Catenin Signaling and Induce Enteric Glial Cell Apoptosis
    Zhan Y, Wen Y, Zheng F, Du LJ, Chen TY, Shen XL, et al.
    Mol Neurobiol, 2024 Mar;61(3):1543-1561.
    PMID: 37728849 DOI: 10.1007/s12035-023-03600-8
    Enteric glial cells (EGCs) are the major component of the enteric nervous system and affect the pathophysiological process of intestinal motility dysfunction. MicroRNAs (miRNAs) play an important role in regulating gastrointestinal homeostasis. However, the mechanism of miRNA-mediated regulation of EGCs in intestinal dysmotility remains unclear. In this study, we investigated the effect of EGC apoptosis on intestinal dysmotility, and the effect of miR-26b-3p on EGC proliferation and apoptosis in vivo and in vitro. A loperamide hydrochloride (Lop)-induced constipated mouse model and an in vitro culture system of rat EGCs were established. The transcriptome was used to predict the differentially expressed gene miR-26b-3p and the target gene Frizzled 10 (FZD10), and their targeting binding relationship was verified by luciferase. EGCs were transfected with miR-26b-3p mimic or antagomir, and the FZD10 expression was down-regulated by siRNA. Immunofluorescence and flow cytometry were used to detect EGC apoptosis. MiR-26b-3p and FZD10 expressions were examined using quantitative real-time PCR (qRT-PCR). The CCK-8 assay was used to detect EGC proliferation. The protein levels were detected by Western blotting and enzyme-linked immunosorbent assay (ELISA). The results showed that miR-26b-3p was up-regulated in the Lop group, whereas FZD10 was down-regulated, and EGC apoptosis was increased in the colon of intestinal dysmotility mice. FZD10 down-regulation and miR-26b-3p mimic significantly increased glycogen synthase kinase-3β phosphorylation (p-GSK3β) levels, decreased β-catenin expression, and promoted EGC apoptosis. MiR-26b-3p antagomir alleviated intestinal dysmotility, promoted EGC increased activity of EGCs, and reduced EGC apoptosis in vivo. In conclusion, this study indicated that miR-26b-3p promotes intestinal motility disorders by targeting FZD10 to block GSK3β/β-catenin signaling and induces apoptosis in EGCs. Our results provide a new research target for the treatment and intervention of intestinal dysmotility.
    Matched MeSH terms: Cell Proliferation
  17. Fulltext New generation of drug delivery systems based on ginsenoside Rh2-, Lysine- and Arginine-treated highly porous graphene for improving anticancer activity
    Zare-Zardini H, Taheri-Kafrani A, Amiri A, Bordbar AK
    Sci Rep, 2018 01 12;8(1):586.
    PMID: 29330486 DOI: 10.1038/s41598-017-18938-y
    In this study, Rh2-treated graphene oxide (GO-Rh2), lysine-treated highly porous graphene (Gr-Lys), arginine-treated Gr (Gr-Arg), Rh2-treated Gr-Lys (Gr-Lys-Rh2) and Rh2-treated Gr-Arg (Gr-Arg-Rh2) were synthesized. MTT assay was used for evaluation of cytotoxicity of samples on ovarian cancer (OVCAR3), breast cancer (MDA-MB), Human melanoma (A375) and human mesenchymal stem cells (MSCs) cell lines. The percentage of apoptotic cells was determined by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay. The hemolysis and blood coagulation activity of nanostructures were performed. Interestingly, Gr-Arg, Gr-Lys, Gr-Arg-Rh2, and Gr-Lys-Rh2 were more active against cancer cell lines in comparison with their cytotoxic activity against normal cell lines (MSCs) with IC50 values higher than 100 μg/ml. The results of TUNEL assay indicates a significant increase in the rates of TUNEL positive cells by increasing the concentrations of nanomaterials. Results were also shown that aggregation and changes of RBCs morphology were occurred in the presence of GO, GO-Rh2, Gr-Arg, Gr-Lys, Gr-Arg-Rh2, and Gr-Lys-Rh2. Note that all the samples had effect on blood coagulation system, especially on PTT. All nanostrucure act as antitumor drug so that binding of drugs to a nostructures is irresolvable and the whole structure enter to the cell as a drug.
    Matched MeSH terms: Cell Proliferation/drug effects
  18. A Real-Time Cell Analyzing Assay for Identification of Novel Antiviral Compounds against Chikungunya Virus
    Zandi K
    Methods Mol Biol, 2016;1426:255-62.
    PMID: 27233278 DOI: 10.1007/978-1-4939-3618-2_23
    Screening of viral inhibitors through induction of cytopathic effects (CPE) by conventional method has been applied for various viruses including Chikungunya virus (CHIKV), a significant arbovirus. However, it does not provide the information about cytopathic effect from the beginning and throughout the course of virus replication. Conventionally, most of the approaches are constructed on laborious end-point assays which are not capable for detecting minute and rapid changes in cellular morphology. Therefore, we developed a label-free and dynamical method for monitoring the cellular features that comprises cell attachment, proliferation, and viral cytopathogenicity, known as the xCELLigence real-time cell analysis (RTCA). In this chapter, we provide a RTCA protocol for quantitative analysis of CHIKV replication using an infected Vero cell line treated with ribavirin as an in vitro model.
    Matched MeSH terms: Cell Proliferation
  19. Fulltext Dietary flavonoid intake and colorectal cancer risk in the European prospective investigation into cancer and nutrition (EPIC) cohort
    Zamora-Ros R, Barupal DK, Rothwell JA, Jenab M, Fedirko V, Romieu I, et al.
    Int J Cancer, 2017 Apr 15;140(8):1836-1844.
    PMID: 28006847 DOI: 10.1002/ijc.30582
    Flavonoids have been shown to inhibit colon cancer cell proliferation in vitro and protect against colorectal carcinogenesis in animal models. However, epidemiological evidence on the potential role of flavonoid intake in colorectal cancer (CRC) development remains sparse and inconsistent. We evaluated the association between dietary intakes of total flavonoids and their subclasses and risk of development of CRC, within the European Prospective Investigation into Cancer and Nutrition (EPIC) study. A cohort of 477,312 adult men and women were recruited in 10 European countries. At baseline, dietary intakes of total flavonoids and individual subclasses were estimated using centre-specific validated dietary questionnaires and composition data from the Phenol-Explorer database. During an average of 11 years of follow-up, 4,517 new cases of primary CRC were identified, of which 2,869 were colon (proximal = 1,298 and distal = 1,266) and 1,648 rectal tumours. No association was found between total flavonoid intake and the risk of overall CRC (HR for comparison of extreme quintiles 1.05, 95% CI 0.93-1.18; p-trend = 0.58) or any CRC subtype. No association was also observed with any intake of individual flavonoid subclasses. Similar results were observed for flavonoid intake expressed as glycosides or aglycone equivalents. Intake of total flavonoids and flavonoid subclasses, as estimated from dietary questionnaires, did not show any association with risk of CRC development.
    Matched MeSH terms: Cell Proliferation/drug effects
  20. The Antimetastatic and Antiangiogenesis Effects of Kefir Water on Murine Breast Cancer Cells
    Zamberi NR, Abu N, Mohamed NE, Nordin N, Keong YS, Beh BK, et al.
    Integr Cancer Ther, 2016 Dec;15(4):NP53-NP66.
    PMID: 27230756
    BACKGROUND: Kefir is a unique cultured product that contains beneficial probiotics. Kefir culture from other parts of the world exhibits numerous beneficial qualities such as anti-inflammatory, immunomodulation, and anticancer effects. Nevertheless, kefir cultures from different parts of the world exert different effects because of variation in culture conditions and media. Breast cancer is the leading cancer in women, and metastasis is the major cause of death associated with breast cancer. The antimetastatic and antiangiogenic effects of kefir water made from kefir grains cultured in Malaysia were studied in 4T1 breast cancer cells.

    METHODS: 4T1 cancer cells were treated with kefir water in vitro to assess its antimigration and anti-invasion effects. BALB/c mice were injected with 4T1 cancer cells and treated orally with kefir water for 28 days.

    RESULTS: Kefir water was cytotoxic toward 4T1 cells at IC50 (half-maximal inhibitory concentration) of 12.5 and 8.33 mg/mL for 48 and 72 hours, respectively. A significant reduction in tumor size and weight (0.9132 ± 0.219 g) and a substantial increase in helper T cells (5-fold) and cytotoxic T cells (7-fold) were observed in the kefir water-treated group. Proinflammatory and proangiogenic markers were significantly reduced in the kefir water-treated group.

    CONCLUSIONS: Kefir water inhibited tumor proliferation in vitro and in vivo mainly through cancer cell apoptosis, immunomodulation by stimulating T helper cells and cytotoxic T cells, and anti-inflammatory, antimetastatic, and antiangiogenesis effects. This study brought out the potential of the probiotic beverage kefir water in cancer treatment.

    Matched MeSH terms: Cell Proliferation/drug effects
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