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Fulltext The modulation of PPARγ1 and PPARγ2 mRNA expression by ciglitazone in CD3/CD28-activated naïve and memory CD4+ T cells

Norazmi MN, Mohamed R, Nurul AA, Yaacob NS

Clin. Dev. Immunol., 2012;2012:849195.
PMID: 22548115 DOI: 10.1155/2012/849195

Given their roles in immune regulation, the expression of the nuclear receptor peroxisome proliferator-activated receptor γ (PPARγ) 1 and 2 isoforms was investigated in human naïve (CD45RA+) and memory (CD45RO+) CD4+ T cells. Stimulation of both types of cells via the CD3/CD28 pathway resulted in high expression of both PPARγ receptors as measured by real-time PCR. Treatment with the PPARγ agonist, ciglitazone, increased PPARγ1 expression but decreased PPARγ2 expression in stimulated naïve and memory cells. Furthermore, when present, the magnitude of both PPARγ receptors expression was lower in naïve cells, perhaps suggesting a lower regulatory control of these cells. Similar profiles of selected proinflammatory cytokines were expressed by the two cell types following stimulation. The induction of PPARγ1 and suppression of PPARγ2 expressions in naïve and memory CD4+ T cells in the presence of ciglitazone suggest that the PPARγ subtypes may have different roles in the regulation of T-cell function.

Matched MeSH terms: Cell Proliferation/drug effects
Strobilanthes crispus inhibits migration, invasion and metastasis in breast cancer

Baraya YS, Wong KK, Yaacob NS

J Ethnopharmacol, 2019 Apr 06;233:13-21.
PMID: 30594607 DOI: 10.1016/j.jep.2018.12.041

ETHNOPHARMACOLOGICAL RELEVANCE: Strobilanthes crispus (L.) Blume, locally known in Malaysia as "Pecah kaca" or "Jin batu", has been traditionally used for treatment of various ailments including cancer. We previously demonstrated that a standardized bioactive subfraction of S. crispus, termed as F3, possessed potent anticancer effects in both in vitro and in vivo breast cancer models.
AIM OF THE STUDY: To investigate the potential of F3 from S. crispus to prevent metastasis in breast cancer.
MATERIALS AND METHODS: The antimetastatic effects of F3 were first investigated on murine 4T1 and human MDA-MB-231 breast cancer cell (BCC) lines using cell proliferation, wound healing and invasion assays. A 4T1-induced mouse mammary carcinoma model was then used to determine the expression of metastasis tumor markers, epithelial (E)-cadherin, matrix metalloproteinase (MMP)-9, mucin (MUC)-1, nonepithelial (N)-cadherin, Twist, vascular endothelial growth factor (VEGF) and vimentin, using immunohistochemistry, following oral treatment with F3 for 30 days.
RESULTS: Significant growth arrest was observed with F3 IC50 values of 84.27 µg/ml (24 h) and 74.41 µg/ml (48 h) for MDA-MB-231, and 87.35 µg/ml (24 h) and 78.75 µg/ml (48 h) for 4T1 cells. F3 significantly inhibited migration of both BCC lines at 50 μg/ml for 24 h (p = 0.018 and p = 0.015, respectively). Similarly, significant inhibition of invasion was demonstrated in 4T1 (75 µg/ml, p = 0.016) and MDA-MB-231 (50 µg/ml, p = 0.040) cells compared to the untreated cultures. F3 treatment resulted in reduced tumor growth compared to untreated mice (p 

Matched MeSH terms: Cell Proliferation/drug effects
The flavonoid fisetin as an anticancer agent targeting the growth signaling pathways

Rengarajan T, Yaacob NS

Eur J Pharmacol, 2016 Oct 15;789:8-16.
PMID: 27377217 DOI: 10.1016/j.ejphar.2016.07.001

Epidemiological studies show that consumption of diets rich in fruits and vegetables is associated with lower risks of cancer. This evidence has kindled interest into research on bioactive food components and has till date resulted in the identification of many compounds with cancer preventive and therapeutic potential. Among such compounds is fisetin (3,7,3,4-tetrahydroxyflavone), a flavonol that is commonly found in many fruits and vegetables such as apples, persimmons, grapes, kiwis, strawberries, onions and cucumbers. Fisetin has been shown to inhibit or retard the growth of various cancer cells in culture and implanted tumors in vivo. Fisetin targets many components of intracellular signaling pathways including regulators of cell survival and apoptosis, tumor angiogenic and metastatic switches by modulating a distinct set of upstream kinases, transcription factors and their regulators. Current evidence supports the idea that fisetin is a promising agent for cancer treatment. This review summarizes reported anticancer effects of fisetin, and re-emphasizes its potential therapeutic role in the treatment of cancer.

Matched MeSH terms: Cell Proliferation/drug effects
Fulltext Berberine Inhibits Telomerase Activity and Induces Cell Cycle Arrest and Telomere Erosion in Colorectal Cancer Cell Line, HCT 116

Samad MA, Saiman MZ, Abdul Majid N, Karsani SA, Yaacob JS

Molecules, 2021 Jan 13;26(2).
PMID: 33450878 DOI: 10.3390/molecules26020376

Colorectal cancer (CRC) is the most common cancer among males and females, which is associated with the increment of telomerase level and activity. Some plant-derived compounds are telomerase inhibitors that have the potential to decrease telomerase activity and/or level in various cancer cell lines. Unfortunately, a deeper understanding of the effects of telomerase inhibitor compound(s) on CRC cells is still lacking. Therefore, in this study, the aspects of telomerase inhibitors on a CRC cell line (HCT 116) were investigated. Screening on HCT 116 at 48 h showed that berberine (10.30 ± 0.89 µg/mL) is the most effective (lowest IC50 value) telomerase inhibitor compared to boldine (37.87 ± 3.12 µg/mL) and silymarin (>200 µg/mL). Further analyses exhibited that berberine treatment caused G0/G1 phase arrest at 48 h due to high cyclin D1 (CCND1) and low cyclin-dependent kinase 4 (CDK4) protein and mRNA levels, simultaneous downregulation of human telomerase reverse transcriptase (TERT) mRNA and human telomerase RNA component (TERC) levels, as well as a decrease in the TERT protein level and telomerase activity. The effect of berberine treatment on the cell cycle was time dependent as it resulted in a delayed cell cycle and doubling time by 2.18-fold. Telomerase activity and level was significantly decreased, and telomere erosion followed suit. In summary, our findings suggested that berberine could decrease telomerase activity and level of HCT 116, which in turn inhibits the proliferative ability of the cells.

Matched MeSH terms: Cell Proliferation/drug effects
Fulltext Safrana l Prevents Prostate Cancer Recurrence by Blocking the Re-activation of Quiescent Cancer Cells via Downregulation of S-Phase Kinase-Associated Protein 2

Jiang X, Li Y, Feng JL, Nik Nabil WN, Wu R, Lu Y, et al.

Front Cell Dev Biol, 2020;8:598620.
PMID: 33392189 DOI: 10.3389/fcell.2020.598620

The re-proliferation of quiescent cancer cells is considered to be the primary contributor to prostate cancer (Pca) recurrence and progression. In this study, we investigated the inhibitory effect of safranal, a monoterpene aldehyde isolated from Crocus sativus (saffron), on the re-proliferation of quiescent Pca cells in vitro and in vivo. The results showed that safranal efficiently blocked the re-activation of quiescent Pca cells by downregulating the G0/G1 cell cycle regulatory proteins CDK2, CDK4, CDK6, and phospho-Rb at Ser807/811 and elevating the levels of cyclin-dependent kinase inhibitors, p21 and p27. Further investigation on the underlying mechanisms revealed that safranal suppressed the mRNA and protein expression levels of Skp2, possibly through the deregulation of the transcriptional activity of two major transcriptional factors, E2F1 and NF-κB subunits. Moreover, safranal inhibited AKT phosphorylation at Ser473 and deregulated both canonical and non-canonical NF-κB signaling pathways. Safranal suppressed the tumor growth of quiescent Pca cell xenografts in vivo. Furthermore, safranal-treated tumor tissues exhibited a reduction in Skp2, E2F1, NF-κB p65, p-IκBα (Ser32), c-MYC, p-Rb (Ser807), CDK4, CDK6, and CDK2 and an elevation of p27 and p21 protein levels. Therefore, our findings demonstrate that safranal suppresses cell cycle re-entry of quiescent Pca cells in vitro and in vivo plausibly by repressing the transcriptional activity of two major transcriptional activators of Skp2, namely, E2F1 and NF-κB, through the downregulation of AKT phosphorylation and NF-κB signaling pathways, respectively.

Matched MeSH terms: Cell Proliferation
Fulltext Saikosaponin A enhances Docetaxel efficacy by selectively inducing death of dormant prostate cancer cells through excessive autophagy

Feng J, Xi Z, Jiang X, Li Y, Nik Nabil WN, Liu M, et al.

Cancer Lett, 2023 Feb 01;554:216011.
PMID: 36442771 DOI: 10.1016/j.canlet.2022.216011

Quiescent cancer cells (QCCs), also known as dormant cancer cells, resist and survive chemo- and radiotherapy, resulting in treatment failure and later cancer recurrence when QCCs resume cell cycle progression. However, drugs selectively targeting QCCs are lacking. Saikosaponin A (SSA) derived from Bupleurum DC., is highly potent in eradicating multidrug-resistant prostate QCCs compared with proliferative prostate cancer cells. By further exacerbating the already increased autophagy through inactivation of Akt-mTOR signaling, SSA triggered cell death in QCCs. Contrarily, inhibition of autophagy or activation of Akt signaling pathway prevented SSA-induced cell death. The multicycle of Docetaxel treatments increased the proportion of QCCs, whereas administering SSA at intervals of Docetaxel treatments aggravated cell death in vitro and led to tumor growth arrest and cell death in vivo. In conclusion, SSA is posed as a novel QCCs-eradicating agent by aggravating autophagy in QCCs. In combination with the current therapy, SSA has potential to improve treatment effectiveness and to prevent cancer recurrence.

Matched MeSH terms: Cell Proliferation
Hydrogel-based methods for engineering cellular microenvironment with spatiotemporal gradients

Wang L, Li Y, Huang G, Zhang X, Pingguan-Murphy B, Gao B, et al.

Crit Rev Biotechnol, 2016 Jun;36(3):553-65.
PMID: 25641330 DOI: 10.3109/07388551.2014.993588

Natural cellular microenvironment consists of spatiotemporal gradients of multiple physical (e.g. extracellular matrix stiffness, porosity and stress/strain) and chemical cues (e.g. morphogens), which play important roles in regulating cell behaviors including spreading, proliferation, migration, differentiation and apoptosis, especially for pathological processes such as tumor formation and progression. Therefore, it is essential to engineer cellular gradient microenvironment incorporating various gradients for the fabrication of normal and pathological tissue models in vitro. In this article, we firstly review the development of engineering cellular physical and chemical gradients with cytocompatible hydrogels in both two-dimension and three-dimension formats. We then present current advances in the application of engineered gradient microenvironments for the fabrication of disease models in vitro. Finally, concluding remarks and future perspectives for engineering cellular gradients are given.

Matched MeSH terms: Cell Proliferation
Human Exfoliated Deciduous Teeth Stem Cells: Features and Therapeutic Effects on Neurogenerative and Hepatobiliary-pancreatic Diseases

Wahab NWA, Guad RM, Subramaniyan V, Fareez IM, Choy KW, Bonam SR, et al.

Curr Stem Cell Res Ther, 2021;16(5):563-576.
PMID: 32957893 DOI: 10.2174/1574888X15999200918105623

Stem cells can multiply into more cells with similar types in an undifferentiated form and differentiate into other types of cells. The great success and key essence of stem cell technology is the isolation of high-quality Mesenchymal Stem Cells (MSCs) with high potency, either with multipotent or pluripotent property. In this line, Stem cells from Human Exfoliated Deciduous teeth (SHEDs) are highly proliferative stem cells from dental pulp and have multipoint differentiation capacity. These cells play a pivotal role in regenerative medicine, such as cell repair associated with neurodegenerative, hepatobiliary, and pancreatic diseases. In addition, stem cell therapy has been widely used to regulate immune response and repair of tissue lesions. This overview captured the differential biological characteristics, and the potential role of stem cell technology and paid special attention to human welfare SHEDs in eliminating the above-mentioned diseases. This review provides further insights into stem cell technology by expanding the therapeutic potential of SHEDs in tissue engineering and cell organ repairs.

Matched MeSH terms: Cell Proliferation
Pd(II) complexes with chelating N-(1-alkylpyridin-4(1H)-ylidene)amide (PYA) ligands: Synthesis, characterization and evaluation of anticancer activity

Zafar MN, Butt AM, Chaudhry GE, Perveen F, Nazar MF, Masood S, et al.

J Inorg Biochem, 2021 11;224:111590.
PMID: 34507110 DOI: 10.1016/j.jinorgbio.2021.111590

The bidentate N-(1-Alkylpyridin-4(1H)-ylidene)amide (PYA) pro-ligands [H2LBn][Cl]2 (2), and [H2LMe][TfO]2 (3) were prepared by simple alkylation reactions of the known compound, N,N-di(pyridin-4-yl)oxalamide (H2L, 1). The Pd(II) complexes, [Pd(LBn)2][Cl]2 (4), [Pd(LMe)2][Cl][TfO] (5), Pd(LBn)Cl2 (6) and Pd(LMe)Cl2 (7) were synthesized through reactions between these pro-ligands and suitable Pd(II) substrates in the presence of base. The molecular structures of 3 and 6 were obtained by single crystal X-ray structure determinations. Studies of the experimental and computational DNA binding interactions of the compounds 1-7 revealed that overall 4 and 6 have the largest values for the binding parameters Kb and ΔGbo. The results showed a good correlation with the steric and electronic parameters obtained by quantitative structure activity relationship (QSAR) studies. In-vitro cytotoxicity studies against four different cell lines showed that the human breast cancer cell lines MCF-7, T47D and cervical cancer cell line HeLa had either higher or similar sensitivities towards 4, 6 and 2, respectively, compared to cisplatin. In general, the cytotoxicity of the compounds, represented by IC50 values, decreased in the order 4 > 6 > 2 > 5 > 3 > 1 > 7 in cancer cell lines. Apoptosis contributed significantly to the cytotoxic effects of these anticancer agents as evaluated by apoptosis studies.

Matched MeSH terms: Cell Proliferation/drug effects
Fulltext Cinnamomum cassia Suppresses Caspase-9 through Stimulation of AKT1 in MCF-7 Cells but Not in MDA-MB-231 Cells

Rad SK, Kanthimathi MS, Abd Malek SN, Lee GS, Looi CY, Wong WF

PLoS One, 2015;10(12):e0145216.
PMID: 26700476 DOI: 10.1371/journal.pone.0145216

BACKGROUND: Cinnamomum cassia bark is a popular culinary spice used for flavoring and in traditional medicine. C. cassia extract (CE) induces apoptosis in many cell lines. In the present study, particular differences in the mechanism of the anti-proliferative property of C. cassia on two breast cancer cell lines, MCF-7 and MDA-MB-231, were elucidated.
METHODOLOGY/PRINCIPAL FINDINGS: The hexane extract of C. cassia demonstrated high anti-proliferative activity against MCF-7 and MDA-MB-231 cells (IC50, 34 ± 3.52 and 32.42 ± 0.37 μg/ml, respectively). Oxidative stress due to disruption of antioxidant enzyme (SOD, GPx and CAT) activity is suggested as the probable cause for apoptosis initiation. Though the main apoptosis pathway in both cell lines was found to be through caspase-8 activation, caspase-9 was also activated in MDA-MB-231 cells but suppressed in MCF-7 cells. Gene expression studies revealed that AKT1, the caspase-9 suppressor, was up-regulated in MCF-7 cells while down-regulated in MDA-MB-231 cells. Although, AKT1 protein expression in both cell lines was down-regulated, a steady increase in MCF-7 cells was observed after a sharp decrease of suppression of AKT1. Trans-cinnamaldehyde and coumarin were isolated and identified and found to be mainly responsible for the observed anti-proliferative activity of CE (Cinnamomum cassia).
CONCLUSION: Activation of caspase-8 is reported for the first time to be involved as the main apoptosis pathway in breast cancer cell lines upon treatment with C. cassia. The double effects of C. cassia on AKT1 gene expression in MCF-7 cells is reported for the first time in this study.

Matched MeSH terms: Cell Proliferation/drug effects*
Fulltext Suppression of cell division-associated genes by Helicobacter pylori attenuates proliferation of RAW264.7 monocytic macrophage cells

Tan GM, Looi CY, Fernandez KC, Vadivelu J, Loke MF, Wong WF

Sci Rep, 2015;5:11046.
PMID: 26078204 DOI: 10.1038/srep11046

Helicobacter pylori at multiplicity of infection (MOI ≥ 50) have been shown to cause apoptosis in RAW264.7 monocytic macrophage cells. Because chronic gastric infection by H. pylori results in the persistence of macrophages in the host's gut, it is likely that H. pylori is present at low to moderate, rather than high numbers in the infected host. At present, the effect of low-MOI H. pylori infection on macrophage has not been fully elucidated. In this study, we investigated the genome-wide transcriptional regulation of H. pylori-infected RAW264.7 cells at MOI 1, 5 and 10 in the absence of cellular apoptosis. Microarray data revealed up- and down-regulation of 1341 and 1591 genes, respectively. The expression of genes encoding for DNA replication and cell cycle-associated molecules, including Aurora-B kinase (AurkB) were down-regulated. Immunoblot analysis verified the decreased expression of AurkB and downstream phosphorylation of Cdk1 caused by H. pylori infection. Consistently, we observed that H. pylori infection inhibited cell proliferation and progression through the G1/S and G2/M checkpoints. In summary, we suggest that H. pylori disrupts expression of cell cycle-associated genes, thereby impeding proliferation of RAW264.7 cells, and such disruption may be an immunoevasive strategy utilized by H. pylori.

Matched MeSH terms: Cell Proliferation
Fulltext MicroRNA 299-3p modulates replicative senescence in endothelial cells

Jong HL, Mustafa MR, Vanhoutte PM, AbuBakar S, Wong PF

Physiol Genomics, 2013 Apr 1;45(7):256-67.
PMID: 23362143 DOI: 10.1152/physiolgenomics.00071.2012

MicroRNAs (miRNAs) regulate various cellular processes. While several genes associated with replicative senescence have been described in endothelial cells, miRNAs that regulate these genes remain largely unknown. The present study was designed to identify miRNAs associated with replicative senescence and their target genes in human umbilical vein endothelial cells (HUVECs). An integrated miRNA and gene profiling approach revealed that hsa-miR-299-3p is upregulated in senescent HUVECs compared with the young cells, and one of its target genes could be IGF1. IGF1 was upregulated in senescent compared with young HUVECs, and knockdown of hsa-miR-299-3p dose-dependently increased the mRNA expression of IGF1, more significantly observed in the presenescent cells (passage 19) compared with the senescent cells (passage 25). Knockdown of hsa-miR-299-3p also resulted in significant reduction in the percentage of cells positively stained for senescence-associated β-galactosidase and increases in cell viability measured by MTT assay but marginal increases in cell proliferation and cell migration capacity measured by real-time growth kinetics analysis. Moreover, knockdown of hsa-miR-299-3p also increased proliferation of cells treated with H2O2 to induce senescence. These findings suggest that hsa-miR-299-3p may delay or protect against replicative senescence by improving the metabolic activity of the senesced cells but does not stimulate growth of the remaining cells in senescent cultures. Hence, these findings provide an early insight into the role of hsa-miR-299-3p in the modulation of replicative senescence in HUVECs.

Matched MeSH terms: Cell Proliferation
Fulltext Squamous epitheliotropism of Enterovirus A71 in human epidermis and oral mucosa

Phyu WK, Ong KC, Kong CK, Alizan AK, Ramanujam TM, Wong KT

Sci Rep, 2017 03 21;7:45069.
PMID: 28322333 DOI: 10.1038/srep45069

Hand-foot-and-mouth disease is a self-limiting paediatric infectious disease commonly caused by Enterovirus A71 (Genus: Enterovirus, Family: Picornaviridae). Typical lesions in and around the hands, feet, oral cavity and other places may rarely be complicated by acute flaccid paralysis and acute encephalomyelitis. Although virus is readily cultured from skin vesicles and oral secretions, the cellular target/s of Enterovirus A71 in human skin and oral mucosa are unknown. In Enterovirus A71-infected human skin and oral mucosa organotypic cultures derived from the prepuce and lip biopsies, focal viral antigens and viral RNA were localized to cytoplasm of epidermal and mucosal squamous cells as early as 2 days post-infection. Viral antigens/RNA were associated with cytoplasmic vacuolation and cellular necrosis. Infected primary prepuce epidermal keratinocyte cultures showed cytopathic effects with concomitant detection of viral antigens from 2 days post-infection. Supernatant and/or tissue homogenates from prepuce skin organotypic cultures and primary prepuce keratinocyte cultures showed viral titres consistent with active viral replication. Our data strongly support Enterovirus A71 squamous epitheliotropism in the human epidermis and oral mucosa, and suggest that these organs are important primary and/or secondary viral replication sites that contribute significantly to oral and cutaneous viral shedding resulting in person-to-person transmission, and viraemia, which could lead to neuroinvasion.

Matched MeSH terms: Cell Proliferation
Cytocompatibility of Titanium Microsphere-Based Surfaces

Huang X, Shan L, Cheng K, Weng W

ACS Biomater Sci Eng, 2017 Dec 11;3(12):3254-3260.
PMID: 33445368 DOI: 10.1021/acsbiomaterials.7b00551

The topography at the micro/nanoscale level for biomaterial surfaces has been thought to play vital roles in their interactions with cells. However, discovering the interdisciplinary mechanisms underlying how cells respond to micro-nanostructured topography features still remains a challenge. In this work, ∼37 μm 3D printing used titanium microspheres and their further hierarchical micro-nanostructured spheres through hydrothermal treatment were adopted to construct typical model surface topographies to study the preosteoblastic cell responses (adhesion, proliferation, and differentiation). We here demonstrated that not only the hierarchical micro-nanostructured surface topography but also their distribution density played critical role on cell cytocompatibility. The microstructured topography feature surface with middle-density distributed titanium microspheres showed significantly enhanced cell responses, which might be attributed to the better cellular interaction due to the cell aggregates. However, the hierarchical micro-nanostructured topography surface, regardless of the distribution density of titanium microspheres, improved the cell-surface interactions because of the enhanced initial protein adsorption, thereby reducing the cell aggregates and consequently their responses. This work, therefore, provides new insights into the fundamental understanding of cell-material interactions and will have a profound impact on further designing micro-nanostructured topography surfaces to control cell responses.

Matched MeSH terms: Cell Proliferation
Wound dressings functionalized with silver nanoparticles: promises and pitfalls

Kalantari K, Mostafavi E, Afifi AM, Izadiyan Z, Jahangirian H, Rafiee-Moghaddam R, et al.

Nanoscale, 2020 Jan 28;12(4):2268-2291.
PMID: 31942896 DOI: 10.1039/c9nr08234d

Infections are the main reason why most people die from burns and diabetic wounds. The clinical challenge for treating wound infections through traditional antibiotics has been growing steadily and has now reached a critical status requiring a paradigm shift for improved chronic wound care. The US Centers for Disease Control have predicted more deaths from antimicrobial-resistant bacteria than from all types of cancers combined by 2050. Thus, the development of new wound dressing materials that do not rely on antibiotics is of paramount importance. Currently, incorporating nanoparticles into scaffolds represents a new concept of 'nanoparticle dressing' which has gained considerable attention for wound healing. Silver nanoparticles (Ag-NPs) have been categorized as metal-based nanoparticles and are intriguing materials for wound healing because of their excellent antimicrobial properties. Ag-NPs embedded in wound dressing polymers promote wound healing and control microorganism growth. However, there have been several recent disadvantages of using Ag-NPs to fight infections, such as bacterial resistance. This review highlights the therapeutic approaches of using wound dressings functionalized with Ag-NPs and their potential role in revolutionizing wound healing. Moreover, the physiology of the skin and wounds is discussed to place the use of Ag-NPs in wound care into perspective.

Matched MeSH terms: Cell Proliferation
A B-myb--DREAM complex is not critical to regulate the G2/M genes in HPV-transformed cell lines

Rashid NN, Yusof R, Watson RJ

Anticancer Res, 2014 Nov;34(11):6557-63.
PMID: 25368258

It is well-established that HPV E7 proteins, encoded by human papillomavirus (HPV) genes, frequently associated with cervical cancers bind avidly to the retinoblastoma (RB) family of pocket proteins and disrupt their association with members of the E2F transcription factor family. Our previous study showed that the repressive p130-dimerization partner, RB-like, E2F and multi-vulval class (DREAM) complex was disrupted by HPV16 E7 proteins in order to maintain the viral replication in CaSki cells. However, we would like to address whether the activator B-myb-DREAM complex is critical in regulating the replication and mitosis phase since our previous study showed increased B-myb-DREAM expression in HPV-transformed cell lines when compared to control cells.

Matched MeSH terms: Cell Proliferation
Disruption of repressive p130-DREAM complexes by human papillomavirus 16 E6/E7 oncoproteins is required for cell-cycle progression in cervical cancer cells

Nor Rashid N, Yusof R, Watson RJ

J Gen Virol, 2011 Nov;92(Pt 11):2620-2627.
PMID: 21813705 DOI: 10.1099/vir.0.035352-0

Human papillomaviruses (HPVs) with tropism for mucosal epithelia are the major aetiological factors in cervical cancer. Most cancers are associated with so-called high-risk HPV types, in particular HPV16, and constitutive expression of the HPV16 E6 and E7 oncoproteins is critical for malignant transformation in infected keratinocytes. E6 and E7 bind to and inactivate the cellular tumour suppressors p53 and Rb, respectively, thus delaying differentiation and inducing proliferation in suprabasal keratinocytes to enable HPV replication. One member of the Rb family, p130, appears to be a particularly important target for E7 in promoting S-phase entry. Recent evidence indicates that p130 regulates cell-cycle progression as part of a large protein complex termed DREAM. The composition of DREAM is cell cycle-regulated, associating with E2F4 and p130 in G0/G1 and with the B-myb transcription factor in S/G2. In this study, we addressed whether p130-DREAM is disrupted in HPV16-transformed cervical cancer cells and whether this is a critical function for E6/E7. We found that p130-DREAM was greatly diminished in HPV16-transformed cervical carcinoma cells (CaSki and SiHa) compared with control cell lines; however, when E6/E7 expression was targeted by specific small hairpin RNAs, p130-DREAM was reformed and the cell cycle was arrested. We further demonstrated that the profound G1 arrest in E7-depleted CaSki cells was dependent on p130-DREAM reformation by also targeting the expression of the DREAM component Lin-54 and p130. The results show that continued HPV16 E6/E7 expression is necessary in cervical cancer cells to prevent cell-cycle arrest by a repressive p130-DREAM complex.

Matched MeSH terms: Cell Proliferation
p38 inhibitor inhibits the apoptosis of cowanin-treated human colorectal adenocarcinoma cells

Chowchaikong N, Nilwarangkoon S, Laphookhieo S, Tanunyutthawongse C, Watanapokasin R

Int J Oncol, 2018 Jun;52(6):2031-2040.
PMID: 29620273 DOI: 10.3892/ijo.2018.4353

Colorectal cancer, which is the third most common type of cancer diagnosed in both men and women, is the leading cause of cancer-related deaths worldwide. Cowanin is a pure compound extracted from Garcinia cowa Roxb., a tree species present in Thailand, Malaysia and Myanmar. The crude extract has been demonstrated to have antitumor activity, inflammation induction, antibacterial activity, anti-inflammatory activity and antimalarial activity. In the present study, the effects of cowanin on apoptosis induction and on the apoptosis-related and mitogen-activated protein kinase (MAPK) pathways were investigated in the LoVo human colorectal cancer cell line. The cytotoxicity of cowanin in LoVo cells was determined by MTT assay. Hoechst 33342 and JC‑1 staining were used to determine nuclear morphological changes and mitochondrial membrane potential, respectively. The expression levels of BCL2 apoptosis regulator (Bcl‑2) family, MAPK and AKT serine/threonine kinase 1 (Akt) pathway proteins following cowanin treatment were determined by western blot analysis. The results demonstrated that cowanin inhibited cell proliferation and induced cell death via the apoptosis pathway. Cowanin treatment increased BCL2 associated X (Bax) and decreased Bcl‑2 expression. In addition, cowanin activated caspase‑9, -7 and poly-ADP-ribose-polymerase expression. Furthermore, cowanin decreased the levels of phosphorylated extracellular signal-regulated kinase (p‑ERK), p‑Akt, p‑3‑phosphoinositide‑dependent protein kinase‑1, while it increased p‑p38 expression, thus resulting in the induction of apoptosis. In conclusion, cowanin inhibited cell proliferation and induced apoptosis of LoVo cells via the MAPK and Akt signaling pathways. Notably, inhibition of p38 by using a p38 inhibitor (SB203580) prevented the cowanin-induced apoptosis in LoVo cells. These results suggested that cowanin may be a potential candidate for the treatment of colorectal cancer and provided important information on the molecular mechanisms underlying its antitumor activity.

Matched MeSH terms: Cell Proliferation/drug effects
Intraductal Carcinoma of Salivary Gland Originating from an Intraparotid Lymph Node: A Case Report

Lin SC, Ko RT, Kang BH, Wang JS

Malays J Pathol, 2019 Aug;41(2):207-211.
PMID: 31427558

INTRODUCTION: Salivary gland intraductal carcinoma (IDC) is rare. We present the second case of IDC originating from an intraparotid lymph node (LN) with a more detailed description of the histogenesis, immunohistochemistry (IHC) and updated molecular information.
CASE REPORT: An 87-year-old male had a tumour nodule over the left parotid tail for about 20 years. Physical examinations revealed a 4.5 cm soft, non-tender and fixed mass. After the left parotidectomy, pathology confirmed the diagnosis of IDC arising within an intraparotid lymph node. The cystic component of the tumour was lined by single to multilayered ductal cells with micropapillary growth pattern. The solid part showed intraductal proliferation of neoplastic cells in solid, cribriform, micropapillary and Roman bridge-like structure. By immunohistochemistry (IHC), the tumour cells were positive for S-100, CK (AE1/AE3), mammaglobin, SOX10, and estrogen receptor (ER), with myoepithelial cell rimming highlighted by positive p63 and calponin IHC stains. The prognosis of this patient is excellent after complete excision.
DISCUSSION: The mechanism of salivary gland tumour arising in the intra-parotid gland LN was assumed to be related to salivary duct inclusion within the intraparotid gland LN which is a normal occurrence during embryology development. Although the terminology may raise some confusion about the relationship between IDC and conventional salivary duct carcinoma (SDA), they are different in immunophenotype and clinicopathologic features. IDC is characterised by S100 (+) ER (+) with predominant intraductal growth and excellent prognosis; while SDC features S100 (-) androgen receptor (+) with predominant invasive growth and aggressive behavior. Recent discovery of recurrent RET gene rearrangement in IDC but not SDC also supports that IDC is not precursor lesion of the SDC.

Matched MeSH terms: Cell Proliferation
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

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