apoptosis https://greenmedinfo.com/category/pharmacological-actions/apoptosis en Anthocyanins work in synergy with trastuzumab by induced apoptosis, inhibited cell growth and affected HER2 downstream signaling. https://greenmedinfo.com/article/anthocyanins-work-synergy-trastuzumab-induced-apoptosis-inhibited-cell-growth- PMID:  Mol Med Rep. 2014 Oct ;10(4):1921-6. Epub 2014 Jul 22. PMID: 25070704 Abstract Title:  Anthocyanins potentiate the activity of trastuzumab in human epidermal growth factor receptor 2-positive breast cancer cells in vitro and in vivo. Abstract:  Human epidermal growth factor receptor 2 (HER2) has been found to be overexpressed in ~25% of invasive breast cancer and is significantly associated with a poor prognosis in breast cancer patients. The anthocyanins cyanidin-3-glucoside (C3G) and peonidin-3-glucoside have been identified as potential drugs for the therapy of HER2‑positive breast cancer. They have been used as supplements in targeted therapeutics and chemotherapeutics in Asia, however, the underlying mechanism remains to be elucidated. The aim of the present study was to investigate the synergism between C3G and trastuzumab (Trast). To address this question, the response to C3G, Trast and a combination of the two drugs, in three representative HER2‑positive cell lines was evaluated. The combination treatments induced apoptosis, inhibited cell growth and affected HER2 and its downstream signaling pathway in MDA‑MB‑453, BT474 and HCC1569 cells, and the effects were synergistic. The combination of 3CG and Trast inhibited tumor growth in an in vivo xenograft model. The data from the present study suggested that C3G exhibits potent antitumor activity when combined with Trast under the investigated conditions. https://greenmedinfo.com/article/anthocyanins-work-synergy-trastuzumab-induced-apoptosis-inhibited-cell-growth-#comments Anthocyanins Breast Cancer: Triple Negative Cyanidin 3-glucoside Anti-Tumor Antiproliferative apoptosis Drug: Trastuzumab Natural Substance/Drug Synergy Supplements Animal Study In Vitro Study Sun, 23 Nov 2014 19:26:57 +0000 greenmedinfo 115283 at https://greenmedinfo.com Astaxanthin exhibits anti-cancer properties in a rat liver cancer cell line. https://greenmedinfo.com/article/astaxanthin-exhibits-anti-cancer-properties-rat-liver-cancer-cell-line PMID:  Toxicol Mech Methods. 2012 Aug 14. Epub 2012 Aug 14. PMID: 22889354 Abstract Title:  Changes in cell ultrastructure and inhibition of JAK1/STAT3 signaling pathway in CBRH-7919 cells with astaxanthin. Abstract:  Abstract Astaxanthin (AST), a xanthophylls carotenoid, possesses significant anticancer effects. However, to date, the molecular mechanism of anticancer remains unclear. In the present research, we studied the anticancer mechanism of AST, including the changes in cell ultrastructure, such as the mitochondrion, rough endoplasmic reticulum (RER), Golgi complex, and cytoskeleton, the inhibition of Janus kinase 1(JAK1)/transduction and the activators of the transcription-3 (STAT3) signaling pathway using rat hepatocellular carcinoma CBRH-7919 cells. Cell apoptosis was evaluated and the expressions of JAK1, STAT3, non-metastasis23-1 (nm23-1), and apoptotic gene like B cell lymphoma/leukemia-2 (bcl-2), B-cell lymphoma-extra large (bcl-xl), proto-oncogene proteins c myc (c-myc) and bcl-2- associated X (bax) were also examined. The results showed that AST could induce cancer cell apoptosis. Under transmission electron microscope, the ultrastructure of treated cells were not clearly distinguishable, the membranes of the mitochondrion, RER, Golgi complex were broken or loosened, and the endoplasmic reticulum (ER) was degranulated. Cytoskeleton depolymerization of the microtubule system led to the collapse of extended vimentin intermediate filament bundles into short agglomerations with disordered distributions. AST inhibited the expression of STAT3, its upstream activator JAK1, and the STAT3 target anti-poptotic genes bcl-2, bcl-xl, and c-myc. Conversely, AST enhanced the expressions of nm23-1 and bax. Overall, our findings demonstrate that AST could induce the apoptosis of CBRH-7919 cells, which are involved in cell ultrastructure and the JAK1/STAT3 signaling pathway. https://greenmedinfo.com/article/astaxanthin-exhibits-anti-cancer-properties-rat-liver-cancer-cell-line#comments Astaxanthin Liver Cancer apoptosis Animal Study Fri, 17 Aug 2012 18:29:02 +0000 greenmedinfo 79629 at https://greenmedinfo.com Curcumin induces apoptosis of triple-negative breast cancer cells. https://greenmedinfo.com/article/curcumin-induces-apoptosis-triple-negative-breast-cancer-cells PMID:  Mol Med Report. 2012 Sep 26. Epub 2012 Sep 26. PMID: 23023821 Abstract Title:  Curcumin induces apoptosis of triple-negative breast cancer cells by inhibition of EGFR expression. Abstract:  Curcumin is the major component of the spice turmeric, extracted from the rhizomes of the plant Curcuma longa. It exerts a number of therapeutic effects, including the inhibition of cancer cell proliferation. However, the anti‑carcinogenic mechanism of curcumin has not been fully elucidated. Triple-negative breast cancer (TNBC), which lacks expression of the estrogen receptor (ER), progesterone receptor (PR) and epidermal growth factor receptor 2 (HER2/EGFR2), is an aggressive breast cancer phenotype with a poor prognosis. In this study, we investigated the effects of curcumin on triple-negative breast cancer cells and the possible molecular mechanisms. The MDA-MB-231 TNBC cells were treated with curcumin, the growth inhibition ratio of the cells was measured by MTT assay, apoptosis was detected by flow cytometryand the expression levels of extracellular regulated protein kinase (ERK1/2), pERK1/2, EGFR and pEGFR were detected by western blotting. After treatment with different concentrations of curcumin, the growth inhibition rates of the MDA-MB-231 breast cancer cells of the 30 µmol/ml curcumin-treatedgroup were significantly different from those of the other groups. The level of apoptosis of the curcumin‑treated group (26.34%) was significantly different from that of the control group (2.76%). The expression levels of pERK1/2 and pEGFR in the curcumin-treated group were significantly decreasedcompared with those of the control group. These results indicate that curcumin is able to inhibit the proliferation of TNBC cells. Inhibition of the EGFR signaling pathway is the likely underlying molecular mechanism. https://greenmedinfo.com/article/curcumin-induces-apoptosis-triple-negative-breast-cancer-cells#comments Breast Cancer: Triple Negative Curcumin apoptosis Epidermal growth factor receptor (EGFR) inhibitor In Vitro Study Tue, 02 Oct 2012 22:16:24 +0000 greenmedinfo 81464 at https://greenmedinfo.com Inhibitory effects of genistein in combination with gefitinib on the hepatocellular carcinoma Hep3B cell line. https://greenmedinfo.com/article/inhibitory-effects-genistein-combination-gefitinib-hepatocellular-carcinoma-he PMID:  Exp Ther Med. 2019 Nov ;18(5):3793-3800. Epub 2019 Sep 19. PMID: 31611933 Abstract Title:  Inhibitory effects of genistein in combination with gefitinib on the hepatocellular carcinoma Hep3B cell line. Abstract:  Combination therapy is an important method for treating advanced hepatocellular carcinoma (HCC). Gefitinib is an epidermal growth factor receptor (EGFR) inhibitor, which has profound effects on HCC. The purpose of the present study was to investigate the effects of genistein in combination with gefitinib on the proliferation and apoptosis of HCC cells and the associated mechanism. Cell counting kit-8 assay was performed to calculate the ICvalues and cytotoxicity, whilst flow cytometry was used to assess cell apoptosis. Protein expression was detected using western blot analysis. The ICof genistein and gefitinib on Hep3B cells were calculated to be 128.078 and 13.657µM, respectively. Genistein in combination with gefitinib significantly inhibited cell viability, promoted apoptosis and reduced EGFR, vascular endothelial growth factor receptor and platelet-derived growth factor receptor phosphorylation. Genistein in combination with gefitinib promoted the expression of cleaved caspase-3 and cleaved poly ADP-ribose polymerase. In addition, combined treatment of genistein and gefitinib strongly inhibited the activation of the Akt/Erk/mTOR signaling pathway. In conclusion, findings from the present study suggest that genistein in combination with gefitinib inhibit HCC cell proliferation and promote apoptosis by inhibiting the Akt/Erk/mTOR pathway. <p><a href="https://greenmedinfo.com/article/inhibitory-effects-genistein-combination-gefitinib-hepatocellular-carcinoma-he" target="_blank">read more</a></p> https://greenmedinfo.com/article/inhibitory-effects-genistein-combination-gefitinib-hepatocellular-carcinoma-he#comments Genistein Liver Cancer Antiproliferative apoptosis Chemotherapeutic Synergy: Gefitinib In Vitro Study Sat, 04 Jan 2020 18:08:44 +0000 greenmedinfo 207099 at https://greenmedinfo.com Olive leaf extract could improve the treatment response of patients with glioblastoma multiforme tumors by modulating miRNA expression. https://greenmedinfo.com/article/olive-leaf-extract-could-improve-treatment-response-patients-glioblastoma-mult PMID:  Am J Cancer Res. 2014 ;4(5):572-90. Epub 2014 Sep 6. PMID: 25232498 Abstract Title:  Olea europaea leaf extract improves the treatment response of GBM stem cells by modulating miRNA expression. Abstract:  The stem-like cells of Glioblastoma multiforme (GBM) tumors (GSCs) are one of the important determinants of recurrence and drug resistance. The aims of the current study were to evaluate the anticancer effect of Olea europaea leaf extract (OLE) on GBM cell lines, the association between OLE and TMZ responses, and the effect of OLE and the OLE-TMZ combination in GSCs and to clarify the molecular mechanism of this effect on the expression of miRNAs related to cell death. The anti-proliferative activity of OLE and the effect of the OLE-TMZ combination were tested in the T98G, U-138MG and U-87MG GBM cell lines using WST-1 assay. The mechanism of cell death was analyzed with Annexin V/FITC and TUNEL assays. The effects of OLE on the expression levels of miR-181b, miR-153, miR-145 and miR-137 and potential mRNA targets were analyzed in GSCs using RT-qPCR. OLE exhibited anti-proliferative effects via apoptosis and necrosis in the GBM cell lines. In addition, OLE significantly induced the expression of miR-153, miR-145, and miR-137 and decreased the expression of the target genes of these miRNAs in GSCs (p https://greenmedinfo.com/article/olive-leaf-extract-could-improve-treatment-response-patients-glioblastoma-mult#comments Glioblastoma Multiforme Olive leaf extract Anti-Proliferative apoptosis Chemopreventive MicroRNA modulator Drug Synergy Significant Treatment Outcome In Vitro Study Thu, 30 Oct 2014 18:10:53 +0000 greenmedinfo 115168 at https://greenmedinfo.com Polyphenols in pomegranate rind could be a potential treatment to suppress bladder cancer cell proliferation. https://greenmedinfo.com/article/polyphenols-pomegranate-rind-could-be-potential-treatment-suppress-bladder-can PMID:  Phytother Res. 2015 Mar ;29(3):415-22. Epub 2015 Jan 8. PMID: 25572695 Abstract Title:  Anti-Proliferative Effects of Polyphenols from Pomegranate Rind (Punica granatum L.) on EJ Bladder Cancer Cells Via Regulation of p53/miR-34a Axis. Abstract:  miRNAs and their validated miRNA targets appear as novel effectors in biological activities of plant polyphenols; however, limited information is available on miR-34a mediated cytotoxicity of pomegranate rind polyphenols in cancer cell lines. For this purpose, cell viability assay, Realtime quantitative PCR for mRNA quantification, western blot for essential protein expression, p53 silencing by shRNA and miR-34a knockdown were performed in the present study. EJ cell treatment with 100 µg (GAE)/mL PRE for 48 h evoked poor cell viability and caspase-dependent pro-apoptosis appearance. PRE also elevated p53 protein and triggered miR-34a expression. The c-Myc and CD44 were confirmed as direct targets of miR-34a in EJ cell apoptosis induced by PRE. Our results provide sufficientevidence that polyphenols in PRE can be potential molecular clusters to suppress bladder cancer cell EJ proliferation via p53/miR-34a axis. Copyright © 2015 John Wiley&amp;Sons, Ltd. https://greenmedinfo.com/article/polyphenols-pomegranate-rind-could-be-potential-treatment-suppress-bladder-can#comments Bladder Cancer Pomegranate Peel Pomegranate Polyphenols Antiproliferative apoptosis MicroRNA modulator Tumor Suppressor Protein p53 Upregulation In Vitro Study Fri, 03 Apr 2015 01:37:31 +0000 greenmedinfo 116605 at https://greenmedinfo.com Red seaweed was more effective than tamoxifen in suppressing tumor growth by 27% with little toxicity to the liver and kidneys. https://greenmedinfo.com/article/red-seaweed-was-more-effective-tamoxifen-suppressing-tumor-growth-27-little-to PMID:  Nutr Cancer. 2013 Feb ;65(2):255-62. PMID: 23441613 Abstract Title:  Comparison of Tamoxifen with Edible Seaweed (Eucheuma cottonii L.) Extract in Suppressing Breast Tumor. Abstract:  The tropical edible red seaweed (Eucheuma cottonii L.) is rich in nutrients and polyphenolic compounds that may suppress cancer through its antioxidant and antiproliferative properties. The study reports on rat mammary tumor suppression and tissue antioxidant status modulation by E. cottonii ethanol extract (ECE). The effect of orally administered ECE (100 mg/kg body-weight) was compared with that of tamoxifen (10 mg/kg body-weight). Rat was induced to develop mammary tumor with subcutaneous injection of LA-7 cells (6 × 10(6) cells/rat). The ECE was more effective than tamoxifen in suppressing tumor growth (27%), improving tissues (plasma, liver,and kidney) malondialdehyde concentrations, superoxide dismutase activity and erythrocyte glutathione concentrations (P&lt;0.05). Unlike tamoxifen, the ECE displayed little toxicity to the liver and kidneys. The ECE exhibited strong anticancer effect with enzyme modulating properties, suggesting its potential as a suppressing agent for mammary gland tumor. https://greenmedinfo.com/article/red-seaweed-was-more-effective-tamoxifen-suppressing-tumor-growth-27-little-to#comments Breast Cancer Antineoplastic Agents Antioxidants Antiproliferative apoptosis Enzyme Modulating Properties Natural Substances Versus Drugs Superiority of Natural Substances versus Drugs Animal Study Wed, 13 Mar 2013 15:38:11 +0000 greenmedinfo 93126 at https://greenmedinfo.com This review focuses on the mechanisms of cannabinoid induced apoptosis and potential therapeutic applications. https://greenmedinfo.com/article/review-focuses-mechanisms-cannabinoid-induced-apoptosis-and-potential-therapeu PMID:  Mini Rev Med Chem. 2005 Jan ;5(1):97-106. PMID: 15638794 Abstract Title:  Involvement of cannabinoids in cellular proliferation. Abstract:  The endogenous canabinoid system (ECS) is involved in the regulation of an important number of central and peripheral physiological effects. Among all these functions, the control of the cellular proliferation has become a focus of major attention as opening new therapeutic possibilities for the use of cannabinoids as potential antitumor agents. The capacity of endogenous and synthetic cannabinoids to induce apoptosis of different tumoral cells in culture and in vivo, the mechanism underlying and the potential therapeutic applications are discussed in this review. https://greenmedinfo.com/article/review-focuses-mechanisms-cannabinoid-induced-apoptosis-and-potential-therapeu#comments Cancers: All Cannabinoids Antiproliferative apoptosis Endogenous Canabinoid System Review Tue, 31 Mar 2015 02:11:14 +0000 greenmedinfo 116545 at https://greenmedinfo.com