Displaying publications 41 - 60 of 1027 in total

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  1. Hashemi M, Sabouni E, Rahmanian P, Entezari M, Mojtabavi M, Raei B, et al.
    Cell Mol Biol Lett, 2023 Apr 21;28(1):33.
    PMID: 37085753 DOI: 10.1186/s11658-023-00438-9
    Hepatocellular carcinoma (HCC) is considered one of the greatest challenges to human life and is the most common form of liver cancer. Treatment of HCC depends on chemotherapy, radiotherapy, surgery, and immunotherapy, all of which have their own drawbacks, and patients may develop resistance to these therapies due to the aggressive behavior of HCC cells. New and effective therapies for HCC can be developed by targeting molecular signaling pathways. The expression of signal transducer and activator of transcription 3 (STAT3) in human cancer cells changes, and during cancer progression, the expression tends to increase. After induction of STAT3 signaling by growth factors and cytokines, STAT3 is phosphorylated and translocated to the nucleus to regulate cancer progression. The concept of the current review revolves around the expression and phosphorylation status of STAT3 in HCC, and studies show that the expression of STAT3 is high during the progression of HCC. This review addresses the function of STAT3 as an oncogenic factor in HCC, as STAT3 is able to prevent apoptosis and thus promote the progression of HCC. Moreover, STAT3 regulates both survival- and death-inducing autophagy in HCC and promotes cancer metastasis by inducing the epithelial-mesenchymal transition (EMT). In addition, upregulation of STAT3 is associated with the occurrence of chemoresistance and radioresistance in HCC. Specifically, non-protein-coding transcripts regulate STAT3 signaling in HCC, and their inhibition by antitumor agents may affect tumor progression. In this review, all these topics are discussed in detail to provide further insight into the role of STAT3 in tumorigenesis, treatment resistance, and pharmacological regulation of HCC.
    Matched MeSH terms: Cell Line, Tumor
  2. Lau MF, Chua KH, Sabaratnam V, Kuppusamy UR
    Sci Prog, 2020;103(1):36850419886448.
    PMID: 31795844 DOI: 10.1177/0036850419886448
    Colorectal cancer is one of the most prevalent noncommunicable diseases worldwide. 5-Fluorouracil is the mainstay of chemotherapy for colorectal cancer. Previously, we have demonstrated that high glucose diminishes the cytotoxicity of 5-fluorouracil by promoting cell cycle progression. The synergistic impact of rosiglitazone on 5-fluorouracil-induced apoptosis was further investigated in this study. Besides control cell lines (CCD-18Co), two human colonic carcinoma cell lines (HCT 116 and HT 29) were exposed to different treatments containing 5-fluorouracil, rosiglitazone or 5-fluorouracil/rosiglitazone combination under normal glucose (5.5 mM) and high-glucose (25 mM) conditions. The cellular oxidative stress level was evaluated with biomarkers of nitric oxide, advanced oxidation protein products, and reduced glutathione. The cell apoptosis was assessed using flow cytometry technique. High glucose caused the production of reduced glutathione in HCT 116 and HT 29 cells. Correspondingly, high glucose suppressed the apoptotic effect of 5-fluorouracil and rosiglitazone. As compared to 5-fluorouracil alone (2 µg/mL), addition of rosiglitazone significantly enhanced the apoptosis (increment rate of 5-20%) in a dose-dependent manner at normal glucose and high glucose levels. This study indicates that high-glucose-induced reduced glutathione confers resistance to apoptosis, but it can be overcome upon treatment of 5-fluorouracil and 5-fluorouracil/rosiglitazone combination. Rosiglitazone may be a promising antidiabetic drug to reduce the chemotherapeutic dose of 5-fluorouracil for colorectal cancer complicated with hyperglycemia.
    Matched MeSH terms: Cell Line, Tumor
  3. Sonam Dongsar T, Tsering Dongsar T, Molugulu N, Annadurai S, Wahab S, Gupta N, et al.
    Environ Res, 2023 Sep 15;233:116455.
    PMID: 37356522 DOI: 10.1016/j.envres.2023.116455
    Breast carcinoma is a molecularly diverse illness, and it is among the most prominent and often reported malignancies in female across the globe. Surgical intervention, chemotherapy, immunotherapy, gene therapy, and endocrine treatment are among the currently viable treatment options for the carcinoma of breast. Chemotherapy is among the most prevalent cancer management strategy. Doxorubicin (DOX) widely employed as a cytostatic medication for the treatment of a variety of malignancies. Despite its widespread acceptance and excellent efficacy against an extensive line up of neoplasia, it has a variety of shortcomings that limit its therapeutic potential in the previously mentioned indications. Employment of nanoparticulate systems has come up as a unique chemo medication delivery strategy and are being considerably explored for the amelioration of breast carcinoma. Polylactic-co-glycolic acid (PLGA)-based nano systems are being utilized in a number of areas within the medical research and medication delivery constitutes one of the primary functions for PLGA given their inherent physiochemical attributes, including their aqueous solubility, biocompatibility, biodegradability, versatility in formulation, and limited toxicity. Herein along with the different application of PLGA-based nano formulations in cancer therapy, the present review intends to describe the various research investigations that have been conducted to enumerate the effectiveness of DOX-encapsulated PLGA nanoparticles (DOX-PLGA NPs) as a feasible treatment option for breast cancer.
    Matched MeSH terms: Cell Line, Tumor
  4. Zulpa AK, Barathan M, Iyadorai T, Mariappan V, Vadivelu J, Teh CSJ, et al.
    World J Microbiol Biotechnol, 2023 Oct 06;39(12):333.
    PMID: 37801157 DOI: 10.1007/s11274-023-03767-1
    pks+ Escherichia coli (E. coli) triggers genomic instability in normal colon cells which leads to colorectal cancer (CRC) tumorigenesis. Previously, we reported a significant presentation of pks+ E. coli strains in CRC patients' biopsies as compared to healthy cohorts. In this work, using an in vitro infection model, we further explored the ability of these strains in modulating cell cycle arrest and activation of apoptotic mediators in both primary colon epithelial cells (PCE) and CRC cells (HCT-116). Sixteen strains, of which eight tumours and the matching non-malignant tissues, respectively, from eight pks+ E. coli CRC patients were subjected to BrDU staining and cell cycle analysis via flow cytometry, while a subset of these strains underwent analysis of apoptotic mediators including caspase proteins, cellular reactive oxygen species (cROS) and mitochondrial membrane potential (MMP) via spectrophotometry as well as proinflammatory cytokines via flow cytometry. Data revealed that all strains exerted S-phase cell cycle blockade in both cells and G2/M phase in PCE cells only. Moreover, more significant upregulation of Caspase 9, cROS, proinflammatory cytokines and prominent downregulation of MMP were detected in HCT-116 cells indicating the potential role of pks related bacterial toxin as anticancer agent as compared to PCE cells which undergo cellular senescence leading to cell death without apparent upregulation of apoptotic mediators. These findings suggest the existence of discrepancies underlying the mechanism of action of pks+ E. coli on both cancer and normal cell lines. This work propounds the rationale to further understand the mechanism underlying pks+ E. coli-mediated CRC tumorigenesis and cancer killing.
    Matched MeSH terms: Cell Line, Tumor
  5. Bhat AA, Afzal O, Afzal M, Gupta G, Thapa R, Ali H, et al.
    Pathol Res Pract, 2024 Jan;253:154991.
    PMID: 38070223 DOI: 10.1016/j.prp.2023.154991
    Lung cancer remains a formidable global health burden, necessitating a comprehensive understanding of the underlying molecular mechanisms driving its progression. Recently, lncRNAs have become necessary controllers of various biological functions, including cancer development. MALAT1 has garnered significant attention due to its multifaceted role in lung cancer progression. Lung cancer, among other malignancies, upregulates MALAT1. Its overexpression has been associated with aggressive tumor behavior and poor patient prognosis. MALAT1 promotes cellular proliferation, epithelial-mesenchymal transition (EMT), and angiogenesis in lung cancer, collectively facilitating tumor growth and metastasis. Additionally, MALAT1 enhances cancer cell invasion by interacting with numerous signaling pathways. Furthermore, MALAT1 has been implicated in mediating drug resistance in lung cancer, contributing to the limited efficacy of conventional therapies. Recent advancements in molecular biology and high-throughput sequencing technologies have offered fresh perspectives into the regulatory networks of MALAT1 in lung cancer. It exerts its oncogenic effects by acting as a ceRNA to sponge microRNAs, thereby relieving their inhibitory effects on target genes. Moreover, MALAT1 also influences chromatin remodeling and post-translational modifications to modulate gene expression, further expanding its regulatory capabilities. This review sheds light on the multifaceted roles of MALAT1 in lung cancer progression, underscoring its potential as an innovative therapeutic target and diagnostic biomarker. Targeting MALAT1 alone or combined with existing therapies holds promise to mitigate lung cancer progression and improve patient outcomes.
    Matched MeSH terms: Cell Line, Tumor
  6. Azizan S, Cheng KJ, Mejia Mohamed EH, Ibrahim K, Faruqu FN, Vellasamy KM, et al.
    Gene, 2024 Feb 20;896:148057.
    PMID: 38043836 DOI: 10.1016/j.gene.2023.148057
    Colorectal cancer (CRC) is ranked as the second leading cause of mortality worldwide, mainly due to metastasis. Epithelial to mesenchymal transition (EMT) is a complex cellular process that drives CRC metastasis, regulated by changes in EMT-associated gene expression. However, while numerous genes have been identified as EMT regulators through various in vivo and in vitro studies, little is known about the genes that are differentially expressed in CRC tumour tissue and their signalling pathway in regulating EMT. Using an integration of systematic search and bioinformatic analysis, gene expression profiles of CRC tumour tissues were compared to non-tumour adjacent tissues to identify differentially expressed genes (DEGs), followed by performing systematic review on common identified DEGs. Fifty-eight common DEGs were identified from the analysis of 82 tumour tissue samples obtained from four gene expression datasets (NCBI GEO). These DEGS were then systematically searched for their roles in modulating EMT in CRC based on previously published studies. Following this, 10 common DEGs (CXCL1, CXCL8, MMP1, MMP3, MMP7, TACSTD2, VIP, HPGD, ABCG2, CLCA4) were included in this study and subsequently subjected to further bioinformatic analysis. Their roles and functions in modulating EMT in CRC were discussed in this review. This study enhances our understanding of the molecular mechanisms underlying EMT and uncovers potential candidate genes and pathways that could be targeted in CRC.
    Matched MeSH terms: Cell Line, Tumor
  7. Hor YZ, Salvamani S, Gunasekaran B, Yian KR
    Yale J Biol Med, 2023 Dec;96(4):511-526.
    PMID: 38161583 DOI: 10.59249/VHYE2306
    Colorectal Neoplasia Differentially Expressed (CRNDE), a long non-coding RNA that was initially identified as aberrantly expressed in colorectal cancer (CRC) has also been observed to exhibit elevated expression in various other human malignancies. Recent research has accumulated substantial evidence implicating CRNDE as an oncogenic player, exerting influence over critical cellular processes linked to cancer progression. Particularly, its regulatory interactions with microRNAs and proteins have been shown to modulate pathways that contribute to carcinogenesis and tumorigenesis. This review will comprehensively outline the roles of CRNDE in colorectal, liver, glioma, lung, cervical, gastric and prostate cancer, elucidating the mechanisms involved in modulating proliferation, apoptosis, migration, invasion, angiogenesis, and radio/chemoresistance. Furthermore, the review highlights CRNDE's potential as a multifaceted biomarker, owing to its presence in diverse biological samples and stable properties, thereby underscoring its diagnostic, therapeutic, and prognostic applications. This review aims to provide comprehensive insights of CRNDE-mediated oncogenesis and identify CRNDE as a promising target for future clinical interventions.
    Matched MeSH terms: Cell Line, Tumor
  8. Holland I, Bakri YM, Sakoff J, Zaleta Pinet D, Motti C, van Altena I
    Phytochemistry, 2021 Aug;188:112798.
    PMID: 34020274 DOI: 10.1016/j.phytochem.2021.112798
    As part of our ongoing study of the specialised metabolites present in brown algae belonging to the Cystophora genus, eight new steroids including three pairs of diastereoisomers were isolated from Cystophora xiphocarpa (Harvey) (Sargassacea, Fucales). The metabolites identified by standard spectrometric methods are (16S,22S)-16,22-dihydroxyergosta-4,24(28)-dien-3-one and (16S,22R)-16,22-dihydroxyergosta-4,24(28)-dien-3-one, (16S,22S,24R)-16,22,24-trihydroxyporifera-4,28-dien-3-one and (16S,22S,24S)-16,22,24-trihydroxystigma-4,28-dien-3-one along with (16S,22S,24E)-16,22-dihydroxystigma-4,24(28)-dien-3-one and (16S,20S)-16,20-dihydroxyergosta-4,24(28)-dien-3-one. (16S,22S,24E)-16,22-Dihydroxystigma-4,24(28)-dien-3-one possessed the most potent cytotoxicity of the steroids in this series with cell growth inhibitions of GI50 8.7 ± 0.7 μM against colon cancer HT29, GI50 5.6 ± 0.8 μM against the breast cancer line MCF-7 and GI50 4.5 ± 0.2 μM against the ovarian cancer cell line A2780. (16S,22R)-16,22-dihydroxyergosta-4,24(28)-dien-3-one was found to be active against the ovarian cancer cell line A2780 with a GI50 of 6.2 ± 0.1 μM.
    Matched MeSH terms: Cell Line, Tumor
  9. de Mendonça IC, Porto IC, do Nascimento TG, de Souza NS, Oliveira JM, Arruda RE, et al.
    BMC Complement Altern Med, 2015 Oct 14;15:357.
    PMID: 26467757 DOI: 10.1186/s12906-015-0888-9
    BACKGROUND: The implementation of new public healthcare models that stimulate the use of natural products from traditional medicine, as a so-called integrated medicine, refers to an approach that use best of both conventional medicine and traditional medicine. Propolis is a widely used natural product by different ancient cultures and known to exhibit biological activities beneficial for health. The large number of studies conducted with propolis had shown that its chemical composition differs as a function of the climate, plant diversity and bee species and plays an important role on its therapeutic properties. The aim of this study was to analyse the phytochemical profile of the ethanolic extract of red propolis (EEP) and its fractionation, antioxidant action of EEP and its fractions hexane, cloroform and ethyl acetate and cytotoxic activity of EEP on human tumour cell lines SF-295 (glioblastoma), OVCAR-8 (ovary) and HCT-116 (colon).

    METHODS: EEP was obtained by maceration with absolute ethanol, then it was concentrated in rotaevaporator up to complete evaporation of the solvent. The crude extract was fractionated with hexane, ethyl acetate, chloroform and methanol and they were subjected to phytochemical screening and total phenolic compounds. Antioxidant activity of EEP and fractions was done by means of the 2,2-diphenyl-1-picryhydrazyl (DPPH) method. Biomarkers of red propolis were identified by LC-Orbitrap-FTMS. To assess cytotoxic activity of the extract, cells were exposed to EEP over 72 h. Cell viability was assessed by means of MTT assay. The percentage of cell growth inhibition (IC50) was analysed by means of non-linear regression, and the absorbance values of the various investigated concentrations were subjected to one-factor analysis of variance (ANOVA) followed by Tukey's or Tamhane's tests (α = 0.05).

    RESULTS: The results obtained using phytochemical screening and LC-Orbitrap-FTMS indicated the presence of phlobaphene tannins, catechins, chalcones, aurones, flavonones, flavonols, xanthones, pentacyclic triterpenoids and guttiferones in Brazilian red propolis. EEP and its hexane, chloroform and ethyl acetate fractions obtained by liquid-liquid partitioning exhibited satisfactory antioxidant percentages. EEP (IC50 cell lines tested when compared to negative control.

    CONCLUSIONS: C-Orbitrap-FTMS was useful to establish the chemical profile of the red propolis. Brazilian red propolis has antioxidant properties and decreases substantially the percentage of cell survival of human tumour cells; thus, it has potential to serve as an anticancer drug.

    Matched MeSH terms: Cell Line, Tumor/drug effects*
  10. Nurhanan MY, Azimahtol Hawariah LP, Mohd Ilham A, Mohd Shukri MA
    Phytother Res, 2005 Nov;19(11):994-6.
    PMID: 16317660 DOI: 10.1002/ptr.1759
    The methanol, n-butanol, chloroform and water extracts obtained from the root of Eurycoma longifolia Jack were assayed using methylene blue assay to evaluate its cytotoxic effect against KB, DU-145, RD, MCF-7, CaOV-3, MDBK cell lines. The results showed that all the root extracts except the water extract of E. longifolia produced significant cytotoxic effect on these cell lines. However, no significant cytotoxic effect was detected on MDBK (kidney) normal cell line. 9-methoxycanthin-6-one, an alkaloid, was detected in each extract with different intensities by reversed-phase high performance liquid chromatography.
    Matched MeSH terms: Cell Line, Tumor/drug effects*
  11. Lee BKB, Gan CP, Chang JK, Tan JL, Fadlullah MZ, Abdul Rahman ZA, et al.
    J Dent Res, 2018 07;97(8):909-916.
    PMID: 29512401 DOI: 10.1177/0022034518759038
    Head and neck cancer (HNC)-derived cell lines represent fundamental models for studying the biological mechanisms underlying cancer development and precision therapies. However, mining the genomic information of HNC cells from available databases requires knowledge on bioinformatics and computational skill sets. Here, we developed a user-friendly web resource for exploring, visualizing, and analyzing genomics information of commonly used HNC cell lines. We populated the current version of GENIPAC with 44 HNC cell lines from 3 studies: ORL Series, OPC-22, and H Series. Specifically, the mRNA expressions for all the 3 studies were derived with RNA-seq. The copy number alterations analysis of ORL Series was performed on the Genome Wide Human Cytoscan HD array, while copy number alterations for OPC-22 were derived from whole exome sequencing. Mutations from ORL Series and H Series were derived from RNA-seq information, while OPC-22 was based on whole exome sequencing. All genomic information was preprocessed with customized scripts and underwent data validation and correction through data set validator tools provided by cBioPortal. The clinical and genomic information of 44 HNC cell lines are easily assessable in GENIPAC. The functional utility of GENIPAC was demonstrated with some of the genomic alterations that are commonly reported in HNC, such as TP53, EGFR, CCND1, and PIK3CA. We showed that these genomic alterations as reported in The Cancer Genome Atlas database were recapitulated in the HNC cell lines in GENIPAC. Importantly, genomic alterations within pathways could be simultaneously visualized. We developed GENIPAC to create access to genomic information on HNC cell lines. This cancer omics initiative will help the research community to accelerate better understanding of HNC and the development of new precision therapeutic options for HNC treatment. GENIPAC is freely available at http://genipac.cancerresearch.my/ .
    Matched MeSH terms: Cell Line, Tumor*
  12. Wong SF, Seow HF, Lai LC
    Malays J Pathol, 2003 Dec;25(2):129-34.
    PMID: 16196369
    Transforming growth factor-beta (TGFbeta) is present, predominantly in latent forms, in normal and malignant breast tissue. The mechanisms by which latent TGFbeta is activated physiologically remain largely an enigma. The objective of this study was to assess whether the proteases, cathepsin D and prostate specific antigen (PSA) could activate latent TGFbeta1 and TGFbeta2 in conditioned media of the hormone-dependent MCF-7 and hormone-independent MDA-MB-231 human breast cancer cell lines, newly purchased from ATCC. Both of the cell lines were seeded in 6-well plates 2 days prior to treatment with varying concentrations of cathepsin D and PSA. Active TGFbeta1 and TGFbeta2 in the media were then measured by ELISA after 4, 8, 24 and 72 hours of treatment. TGFbeta1 and TGFbeta2 mRNA expression of both cell lines were measured by RT-PCR to determine whether any increase in level of active TGFbeta1 and TGFbeta2 was due to increased production. There was a significant increase in only active TGFbeta2 levels in the MDA-MB-231 cell line with both treatments. Cathepsin D and PSA did not have any effect on TGFbeta1 and TGFbeta2 mRNA expression. Cathepsin D and PSA were unable to activate latent TGFbeta1 and TGFbeta2 in these two breast cancer cell lines. A constant level of TGFbeta2 mRNA in the control and treated MDA-MB-231 cells suggests that the increase in level of active TGFbeta2 was not a result of increased production but was likely to be due to activation by a mechanism independent of cathepsin D and PSA.
    Matched MeSH terms: Cell Line, Tumor/drug effects; Cell Line, Tumor/metabolism
  13. Wong CC, Periasamy N, Sagineedu SR, Sidik S, Sumon SH, Loadman P, et al.
    Invest New Drugs, 2014 Oct;32(5):806-14.
    PMID: 24875131 DOI: 10.1007/s10637-014-0105-6
    Limited tumor penetrability of anti-cancer drugs is recognized as one of the major factors that lead to poor anti-tumor activity. SRJ09 (3,19-(2-bromobenzylidene) andrographolide) has been identified as a lead anti-cancer agent for colon cancer. Recently, this compound was shown by us to be a mutant K-Ras binder. In this present study, the penetrability of SRJ09 through the DLD-1 colon cancer multicell layer (MCL) was evaluated. The amount of SRJ09 that penetrated through the MCL was quantitated by utilizing high performance liquid chromatography (HPLC). Histopathological staining was used to visualize the morphology of MCL. A chemosensitivity assay was performed to assess the anti-cancer activity of SRJ09 in DLD-1 cells. SRJ09 was able to penetrate through DLD-1 MCL and is inversely proportional with the MCL thickness. The flow rates for SRJ09 through MCL were 0.90 ± 0.20 μM/min/cm(2) and 0.56 ± 0.06 μM/min/cm(2) for days 1 and 5, respectively, which are better than doxorubicin. Histopathological examination revealed that the integrity of the DLD-1 MCL was retained and no visible damage was inflicted on the cell membrane, confirming the penetration of SRJ09 was by diffusion. Short term exposure (1 h) in DLD-1 cells demonstrated SRJ09 had IC50 of 41 μM which was approximately 4-folds lower than andrographolide, the parent compound of SRJ09. In conclusion, SRJ09 successfully penetrated through DLD-1 MCL by diffusion and emerged as a potential candidate to be developed as a clinically viable anti-colon cancer drug.
    Matched MeSH terms: Cell Line, Tumor
  14. Akhtar MN, Zareen S, Yeap SK, Ho WY, Lo KM, Hasan A, et al.
    Molecules, 2013 Aug 20;18(8):10042-55.
    PMID: 23966087 DOI: 10.3390/molecules180810042
    Naturally occurring anthraquinones, damnacanthal (1) and nordamnacanthal (2) were synthesized with modified reaction steps and investigated for their cytotoxicity against the MCF-7 and K-562 cancer cell lines, respectively. Intermediate analogues 2-bromomethyl-1,3-dimethoxyanthraquinone (5, IC50 = 5.70 ± 0.21 and 8.50 ± 1.18 mg/mL), 2-hydroxymethyl-1,3-dimethoxyanthraquinone (6, IC50 = 12.10 ± 0.14 and 14.00 ± 2.13), 2-formyl-1,3-dimethoxyantharquinone (7, IC50 = 13.10 ± 1.02 and 14.80 ± 0.74), 1,3-dimethoxy-2-methylanthraquinone (4, IC50 = 9.40 ± 3.51 and 28.40 ± 2.33), and 1,3-dihydroxy-2-methylanthraquinone (3, IC50 = 25.60 ± 0.42 and 28.40 ± 0.79) also exhibited moderate cytotoxicity against MCF-7 and K-562 cancer cell lines, respectively. Other structurally related compounds like 1,3-dihydroxyanthraquinone (13a, IC50 = 19.70 ± 0.35 and 14.50 ± 1.28), 1,3-dimethoxyanthraquinone (13b, IC50 = 6.50 ± 0.66 and 5.90 ± 0.95) were also showed good cytotoxicity. The target compound damnacanthal (1) was found to be the most cytotoxic against the MCF-7 and K-562 cancer cell lines, with IC50 values of 3.80 ± 0.57 and 5.50 ± 1.26, respectively. The structures of all compounds were elucidated with the help of detailed spectroscopic techniques.
    Matched MeSH terms: Cell Line, Tumor
  15. Althunibat OY, Ridzwan BH, Taher M, Daud JM, Jauhari Arief Ichwan S, Qaralleh H
    Acta. Biol. Hung., 2013 Mar;64(1):10-20.
    PMID: 23567827 DOI: 10.1556/ABiol.64.2013.1.2
    Sea cucumbers are marine invertebrates of the phylum of Echinodermata that have been used in Asian traditional medicine since ancient times. This study was conducted to investigate the antioxidant and cytotoxic properties of aqueous and organic extracts from two sea cucumber species, Holothuria edulis Lesson (Holothuriidae) and Stichopus horrens Selenka (Stichopodidae). Antioxidant activities of the extracts were evaluated by DPPH· and β-carotene bleaching assays, while MTT and trypan blue exclusion assays were used to demonstrate the cytotoxic effects of the extracts against two human cancer cell lines, non-small cell lung cancer cells (A549) and esophageal cancer cells (TE1). The results showed that both aqueous and organic extracts of H. edulis were able to scavenge DPH radical (IC50 at 2.04 mg/ml and 8.73 mg/ml, respectively). Aqueous and organic extracts of S. horrens inhibited 79.62% and 46.66% of β-carotene oxidation by linoleate free radical. On the other hand, the organic extract of S. horrens exhibited the highest cytotoxic effects against A549 and TE1 cancer cells giving IC50 at 15.5 and 4.0 μg/ml, respectively. In conclusion, the present study revealed that H. edulis and S. horrens contain promising levels of antioxidant and cytotoxic natural products that might be used for cancer prevention and treatment.
    Matched MeSH terms: Cell Line, Tumor
  16. Yue TH, Hock AH, Kiang LC, Mooi LY
    Nat Prod Commun, 2012 Jun;7(6):775-8.
    PMID: 22816305
    Phytochemical studies of the leaves and rhizomes of Paraboea pa niculata (Gesneriaceae) are reported for the first time. Three phenylethanoid glycosides were isolated and characterized as 3,4-dihydroxyphenethyl-(3"-O-beta-D-apiofuranosyl)-beta-D-glucopyranoside, calceoralarioside E, and acteoside. These isolates exhibited weak cytotoxic activity against the K-562 cell line with a 50% of cell killing rate of 40.18 microM, 27.05 microM, and 27.24 microM, respectively. In the DPPH free radical scavenging assay, their IC50 values were determined as 75.89 microM, 25.00 microM, and 26.04 microM, respectively.
    Matched MeSH terms: Cell Line, Tumor
  17. Tang SW, Sukari MA, Rahmani M, Lajis NH, Ali AM
    Molecules, 2011 Apr 07;16(4):3018-28.
    PMID: 21475124 DOI: 10.3390/molecules16043018
    A new abietene diterpene, kaempfolienol (5S,6S,7S,9S,10S,11R,13S-abiet-8(14)-enepenta-6,7,9,11,13-ol, 1), was isolated from a rhizome extract of Kaempferia angustifolia Rosc. along with the known compounds crotepoxide, boesenboxide, zeylenol, 2'-hydroxy-4,4',6'-trimethoxychalcone, (24S)-24-methyl-5α-lanosta-9(11),25-dien-3β-ol, β-sitosterol and β-sitosterol-3-O-β-D-glucopyranoside. The structures of all compounds were elucidated on the basis of mass spectroscopic and NMR data. Zeylenol (2), the major constituent of the plant, was derivatized into diacetate, triacetate and epoxide derivatives through standard organic reactions. The cytotoxic activity of compounds 1, 2 and the zeylenol derivatives was evaluated against the HL-60, MCF-7, HT-29 and HeLa cell lines.
    Matched MeSH terms: Cell Line, Tumor
  18. Aspollah Sukari M, Wah TS, Saad SM, Rashid NY, Rahmani M, Lajis NH, et al.
    Nat Prod Res, 2010 May;24(9):838-45.
    PMID: 20461629 DOI: 10.1080/14786410903052951
    Curcuma ochrorhiza ('temu putih') and C. heyneana ('temu giring') are two Zingiberaceous species which are commonly used in traditional medicine in Malaysia and Indonesia. Phytochemical investigations on these Curcuma species have resulted in the isolation of six sesquiterpenes, namely zerumbone (1), furanodienone (2), zederone (3), oxycurcumenol epoxide (4), curcumenol (5) and isocurcumenol (6), along with phytosterols stigmasterol and alpha-sitosterol. Compounds 1 and 2 were obtained for the first time for C. ochrorhiza while 4 was new to C. heyneana. The hexane extract of C. ochrorhiza and sesquiterpenes 1 and 3 showed very strong cytotoxicity activity against T-acute lymphoblastic leukaemia cells (CEM-SS), with IC(50) values of 6.0, 0.6 and 1.6 microg mL(-1), respectively. Meanwhile, constituents from C. heyneana (4-6) demonstrated moderate inhibition against CEM-SS in cytotoxic assay, with IC(50) values of 11.9, 12.6 and 13.3 microg mL(-1), respectively. The crude extracts and sesquiterpenes isolated were moderately active against certain bacteria tested in antimicrobial screening.
    Matched MeSH terms: Cell Line, Tumor
  19. Malek SN, Phang CW, Ibrahim H, Norhanom AW, Sim KS
    Molecules, 2011 Jan 14;16(1):583-9.
    PMID: 21240148 DOI: 10.3390/molecules16010583
    The methanol and fractionated extracts (hexane, ethyl acetate and water) of Alpinia mutica (Zingiberaceae) rhizomes were investigated for their cytotoxic effect against six human carcinoma cell lines, namely KB, MCF7, A549, Caski, HCT116, HT29 and non-human fibroblast cell line (MRC 5) using an in vitro cytotoxicity assay. The ethyl acetate extract possessed high inhibitory effect against KB, MCF7 and Caski cells (IC₅₀ values of 9.4, 19.7 and 19.8 µg/mL, respectively). Flavokawin B (1), 5,6-dehydrokawain (2), pinostrobin chalcone (3) and alpinetin (4), isolated from the active ethyl acetate extract were also evaluated for their cytotoxic activity. Of these, pinostrobin chalcone (3) and alpinetin (4) were isolated from this plant for the first time. Pinostrobin chalcone (3) displayed very remarkable cytotoxic activity against the tested human cancer cells, such as KB, MCF7 and Caski cells (IC₅₀ values of 6.2, 7.3 and 7.7 µg/mL, respectively). This is the first report of the cytotoxic activity of Alpinia mutica.
    Matched MeSH terms: Cell Line, Tumor
  20. Awang K, Hadi AH, Saidi N, Mukhtar MR, Morita H, Litaudon M
    Fitoterapia, 2008 Jun;79(4):308-10.
    PMID: 18313862 DOI: 10.1016/j.fitote.2007.11.025
    The bark of Cryptocarya crassinervia provided two new phenantrene alkaloids, 2-hydroxyatherosperminine (1) and N-demethyl-2-methoxyatherosperminine (2).
    Matched MeSH terms: Cell Line, Tumor
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