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Simvastatin prevents BMP-2 driven cell migration and invasion by suppressing oncogenic DNMT1 expression in breast cancer cells
This study emphasized to decipher the molecular mechanism of endogenous regulation of DNMT1 expression for finding upstream signaling molecules. Cancer database analyses found an upregulated DNMT1 expression in most cancer types including breast cancer. Overexpression of DNMT1 showed an increased cell migration, invasion, and stemness potential whereas 5-azacytidine (DNMT1 inhibitor) and siRNA mediated knockdown of DNMT1 exhibited inhibition of such cancer activities in breast cancer MDA-MB-231 and MCF-7 cells. Infact, cancer database analyses further found a positive correlation of DNMT1 transcript with both cholesterol p...
Source: Gene - July 13, 2023 Category: Genetics & Stem Cells Authors: Pooja Yadav Shreetama Bandyopadhayaya Sneha Soni Sunil Saini Lokendra K Sharma Sandeep K Shrivastava Chandi C Manda Source Type: research

Simvastatin Suppresses Human Breast Cancer Cell Invasion by Decreasing the Expression of Pituitary Tumor-Transforming Gene 1
Statins, or 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors, have been widely used to lower cholesterol and prevent cardiovascular diseases. Recent preclinical and clinical studies have shown that statins exert beneficial effects in the management of breast cancer, while the underlying mechanisms remain to be elucidated. Herein, we sought to investigate the effect of statins on the expression of pituitary tumor-transforming gene 1 (PTTG1), a critical gene involved in human breast cancer invasion and metastasis. Our results showed that PTTG1 is highly expressed in malignant Hs578T and MDA-MB-231 breast cancer cel...
Source: Frontiers in Pharmacology - November 4, 2020 Category: Drugs & Pharmacology Source Type: research

Combination simvastatin and metformin synergistically inhibits endometrial cancer cell growth.
CONCLUSIONS: MET+SIM treatment synergistically inhibits endometrial cancer cell viability. This may be mediated by apoptosis and mTOR pathway inhibition. Our results provide preclinical evidence that the combination of these well-tolerated drugs may warrant further clinical investigation for endometrial cancer treatment. PMID: 31178149 [PubMed - as supplied by publisher]
Source: Gynecologic Oncology - June 5, 2019 Category: Cancer & Oncology Authors: Kim JS, Turbov J, Rosales R, Thaete LG, Rodriguez GC Tags: Gynecol Oncol Source Type: research

OPN b and c Isoforms Doubtless Veto Anti-angiogenesis Effects of Curcumin in Combination with Conventional AML Regiment
Authors: Mirzaei A, Ghaffari SH, Nikbakht M, Kamranzadeh Foumani H, Vaezi M, Mohammadi S, Alimoghaddam K, Ghavamzadeh A Abstract Osteopontin (OPN) is an extracellular structural protein that is secreted by osteoblasts and hematopoietic cells. It suppresses the proliferation of hematopoietic stem and also plays an important role in promoting survival and drug resistance in leukemic stem cells (LSCs). Since the role of OPN isoforms in AML angiogenesis are remaining controversial, in the present study, we aimed to evaluate whether curcumin (CUR), as a known natural component with anti-angiogenesis effects, in a combin...
Source: Asian Pacific Journal of Cancer Prevention - September 29, 2017 Category: Cancer & Oncology Tags: Asian Pac J Cancer Prev Source Type: research

Simvastatin Up ‐Regulates Annexin A10 That Can Inhibit the Proliferation, Migration, and Invasion in Androgen‐Independent Human Prostate Cancer Cells
CONCLUSIONOur results suggest that statins inhibit the proliferation, migration, and invasion of androgen‐independent prostate cancer cells by up‐regulation of ANXA10. Additionally, it is possible that S100A4 plays a role in these effects. Statins may be beneficial in the prevention and/or treatment of prostate cancer. Prostate © 2016 Wiley Periodicals, Inc.
Source: The Prostate - November 7, 2016 Category: Urology & Nephrology Authors: Yoshiyuki Miyazawa, Yoshitaka Sekine, Haruo Kato, Yosuke Furuya, Hidekazu Koike, Kazuhiro Suzuki Tags: Original Article Source Type: research

The apoptotic effect of simvastatin via the upregulation of BIM in nonsmall cell lung cancer cells.
CONCLUSIONS: Simvastatin restored the expression of BIM to induce apoptotic cell death in NSCLC cells harboring an EGFR-resistant mutation. Our study suggests the potential utility of simvastatin as a BIM-targeted treatment for NSCLC. PMID: 26756263 [PubMed - in process]
Source: Experimental Lung Research - February 18, 2016 Category: Respiratory Medicine Tags: Exp Lung Res Source Type: research

Inhibition of autophagy potentiates pemetrexed and simvastatin-induced apoptotic cell death in malignant mesothelioma and non-small cell lung cancer cells
In this study, we determined whether autophagy could be induced by pemetrexed and simvastatin cotreatment in malignant mesothelioma and NSCLC cells. Furthermore, we determined whether inhibition of autophagy drives apoptosis in malignant mesothelioma and NSCLC cells. Malignant mesothelioma MSTO-211H and A549 NSCLC cells were treated with pemetrexed and simvastatin alone and in combination to evaluate their effect on autophagy and apoptosis. Cotreatment with pemetrexed and simvastatin induced greater caspase-dependent apoptosis and autophagy than either drug alone in malignant mesothelioma and NSCLC cells. 3-Methyladenine (...
Source: European Respiratory Journal - October 30, 2015 Category: Respiratory Medicine Authors: Kim, H.-R., Cho, K.-H., Hwang, K.-E., Jeong, E.-T. Tags: 11.1 Lung Cancer Source Type: research

Simvastatin protects Sertoli cells against cisplatin cytotoxicity through enhanced gap junction intercellular communication.
Authors: Wang L, Peng J, Huang H, Wang Q, Yu M, Tao L Abstract Cisplatin, an important chemotherapeutic agent against testicular germ cell cancer, induces testicular toxicity on Leydig and Sertoli cells, leading to serious side-effects such as azoospermia and infertility. In a previous study, it was found that simvastatin enhanced the sensitivity of Leydig tumor cells to chemotherapeutic toxicity through the enhancement of gap junction functions. In the present study, the effect of simvastatin on the sensitivity of normal Sertoli cells to cisplatin and the role of gap junctions in such effects was investigated. T...
Source: Oncology Reports - August 15, 2015 Category: Cancer & Oncology Tags: Oncol Rep Source Type: research

Abstract 16: Combination simvastatin and metformin induces G1-phase cell cycle arrest and Ripk1- and Ripk3-dependent necroptosis in C4-2B osseous metastatic castration-resistant prostate cancer cells
Castration-resistant prostate cancer (CRPC) cells acquire resistance to chemotherapy and apoptosis in part due to enhanced aerobic glycolysis and biomass production, known as Warburg effect. We previously demonstrated that combination simvastatin (SIM) and metformin (MET) ameliorates critical Warburg effect-related metabolic aberrations of C4-2B cells, synergistically and significantly decreases CRPC cell viability and metastatic properties, with minimal effect on normal prostate epithelial cells, and inhibits primary prostate tumor growth, metastasis, and biochemical failure in an orthotopic model of metastatic CRPC, more...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Babcook, M. A., Sramkoski, R. M., Fujioka, H., Daneshgari, F., Almasan, A., Shukla, S., Gupta, S. Tags: Molecular and Cellular Biology Source Type: research

Synergistic Effect of Sulindac and Simvastatin on Apoptosis in Lung Cancer A549 Cells through ...
Conclusion Combined treatment with sulindac and simvastatin augmented their apoptotic potential in lung cancer cells through AKT signaling-dependent downregulation of survivin. These results indicate that sulindac and simvastatin may be clinically promising therapies for the prevention of lung cancer.
Source: Cancer Research and Treatment - October 26, 2014 Category: Cancer & Oncology Tags: Original Article Source Type: research

Effect of simvastatin on the resistance to EGFR tyrosine kinase inhibitors in a non-small cell lung cancer with the T790M mutation of EGFR.
This study investigated overcoming resistance to EGFR-TKI using simvastatin. We demonstrated that addition of simvastatin to gefitinib enhanced caspase-dependent apoptosis in T790M mutant NSCLC cells. Simvastatin also strongly inhibited AKT activation, leading to suppression of β-catenin activity and the expression of its targets, survivin and cyclin D1. Both insulin treatment and AKT overexpression markedly increased p-β-catenin and survivin levels, even in the presence of gefitinib and simvastatin. However, inhibition of AKT by siRNA or LY294002 treatment decreased p-β-catenin and survivin levels. To determine the rol...
Source: Experimental Cell Research - March 12, 2014 Category: Cytology Authors: Hwang KE, Kwon SJ, Kim YS, Park DS, Kim BR, Yoon KH, Jeong ET, Kim HR Tags: Exp Cell Res Source Type: research

Simvastatin inhibition of mevalonate pathway induces apoptosis in human breast cancer cells via activation of JNK/CHOP/DR5 signaling pathway
Highlights: ► Lipophilic statin, simvastatin, triggers apoptosis in human breast cancer cells via JNK/CHOP/DR5 dependent signaling. ► Simvastatin blockage of mevalonate and geranylgeranyl pyrophosphate is critical for pro-death effect. ► Death Receptor 5 protein levels are upregulated by simvastatin and necessary for simvastatin-induced apoptosis.Abstract: Simvastatin (SVA) was shown to up-regulate expression of death receptor-5 (DR5), CCAAT/enhancer binding protein homologous protein (CHOP) and phosphorylated c-Jun N-terminal kinase (pJNK) in human breast cancer cell lines. siRNA knockdown of DR5, CHOP or JNK signif...
Source: Cancer Letters - December 7, 2012 Category: Cancer & Oncology Authors: Archana Gopalan, Weiping Yu, Bob G. Sanders, Kimberly Kline Tags: Research Articles Source Type: research