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Cancer: Prostate Cancer
Drug: Metformin

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Total 21 results found since Jan 2013.

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

The interplay of AMP‐activated protein kinase and androgen receptor in prostate cancer cells
Abstract AMP‐activated protein kinase (AMPK) has recently emerged as a potential target for cancer therapy due to the observation that activation of AMPK inhibits tumor cell growth. It is well‐known that androgen receptor (AR) signaling is a major driver for the development and progression of prostate cancer and that downregulation of AR is a critical step in the induction of apoptosis in prostate cancer cells. However, little is known about the potential interaction between AMPK and AR signaling pathways. In the current study, we showed that activation of AMPK by metformin caused decrease of AR protein level through s...
Source: Journal of Cellular Physiology - October 17, 2013 Category: Cytology Authors: Min Shen, Zhen Zhang, Manohar Ratnam, Q. Ping Dou Tags: Rapid Communication Source Type: research

Metformin anti-tumor effect via disruption of the MID1 translational regulator complex and AR downregulation in prostate cancer cells
Conclusions: Findings reported herein uncover a mechanism for the anti-tumor activity of metformin in prostate cancer, which is independent of its anti-diabetic effects. These data provide a rationale for the use of metformin in the treatment of hormone naive and castration-resistant prostate cancer and suggest AR is an important indirect target of metformin.
Source: BMC Cancer - January 31, 2014 Category: Cancer & Oncology Authors: Ummuhan DemirAndrea KoehlerRainer SchneiderSusann SchweigerHelmut Klocker Source Type: research

Role of AMPK in Regulating EMT
In cancer cells, the epithelial–mesenchymal transition (EMT) confers the ability to invade basement membranes and metastasize to distant sites, establishing it as an appealing target for therapeutic intervention. Here, we report a novel function of the master metabolic kinase AMPK in suppressing EMT by modulating the Akt–MDM2–Foxo3 signaling axis. This mechanistic link was supported by the effects of siRNA-mediated knockdown and pharmacologic activation of AMPK on epithelial and mesenchymal markers in established breast and prostate cancer cells. Exposure of cells to OSU-53, a novel allosteric AMPK activator, as well...
Source: Cancer Research - September 1, 2014 Category: Cancer & Oncology Authors: Chou, C.-C., Lee, K.-H., Lai, I.-L., Wang, D., Mo, X., Kulp, S. K., Shapiro, C. L., Chen, C.-S. Tags: Therapeutics, Targets, and Chemical Biology Source Type: research

Metformin inhibits the proliferation of human prostate cancer PC-3 cells via the downregulation of insulin-like growth factor 1 receptor.
Abstract Metformin is a biguanide drug that is widely used for the treatment of type 2 diabetes. Recent studies have shown that metformin inhibits cancer cell proliferation and tumor growth both in vitro and in vivo. The anti-tumor mechanisms of metformin include activation of the AMP-activated protein kinase/mTOR pathway and direct inhibition of insulin/insulin-like growth factor (IGF)-mediated cellular proliferation. However, the anti-tumor mechanism in prostate cancer remains unclear. Because activation of the IGF-1 receptor (IGF-1R) is required for prostate cell proliferation, IGF-1R inhibitors may be of the...
Source: Biochemical and Biophysical Research communications - April 7, 2015 Category: Biochemistry Authors: Kato H, Sekine Y, Furuya Y, Miyazawa Y, Koike H, Suzuki K Tags: Biochem Biophys Res Commun 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

Abstract 3814: Metformin induces ER stress-dependent apoptosis through miR-708-5p/NNAT pathway in prostate cancer
In this study, we identified miR-708-5p as a novel downstream effector of metformin in prostate cancer. By increasing the expression of miR-708-5p, metformin suppresses the expression of endoplasmic reticulum (ER) membrane protein neuronatin (NNAT) and subsequently induces apoptosis of prostate cancer cells through ER stress pathway. Notably, down-regulated NNAT is associated with down-regulated intracellular calcium level and induces malformation of endoplasmic reticulum-ribosome structure which is revealed by electronic microscopy. Furthermore, western blot shows that the unfolded-protein response (UPR) proteins includin...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Yang, J., Wei, J., Wu, Y., Wang, Z., Guo, Y., Li, X. Tags: Molecular and Cellular Biology Source Type: research

Abstract 4969: Metformin causes AR degradation via Skp2-mediated ubiquitination
This study supports that use of metformin in combination with Enza or other ARSI drugs may not only block autophagy survival but also cause AR degradation that leads to PC cell death.Citation Format: Joy C. Yang, Allen C. Gao, Christopher P. Evans. Metformin causes AR degradation via Skp2-mediated ubiquitination. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 4969. doi:10.1158/1538-7445.AM2015-4969
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Yang, J. C., Gao, A. C., Evans, C. P. Tags: Molecular and Cellular Biology Source Type: research

Metformin elicits antitumor effects and downregulates the histone methyltransferase multiple myeloma SET domain (MMSET) in prostate cancer cells
CONCLUSIONSThese data suggest MMSET may play a role in the inhibitory effect of metformin on PCa and could serve as a potential novel therapeutic target for PCa. Prostate © 2016 Wiley Periodicals, Inc.
Source: The Prostate - July 11, 2016 Category: Urology & Nephrology Authors: Nicole M. A. White‐Al Habeeb, Julia Garcia, Neil Fleshner, Bharati Bapat Tags: Original Article Source Type: research

Hyperglycaemia-induced resistance to Docetaxel is negated by metformin: a role for IGFBP-2
The incidence of many common cancers varies between different populations and appears to be affected by a Western lifestyle. Highly proliferative malignant cells require sufficient levels of nutrients for their anabolic activity. Therefore, targeting genes and pathways involved in metabolic pathways could yield future therapeutics. A common pathway implicated in energetic and nutritional requirements of a cell is the LKB1/AMPK pathway. Metformin is a widely studied anti-diabetic drug, which improves glycaemia in patients with type 2 diabetes by targeting this pathway. We investigated the effect of metformin on prostate can...
Source: Endocrine-Related Cancer - November 20, 2016 Category: Endocrinology Authors: Biernacka, K. M., Persad, R. A., Bahl, A., Gillatt, D., Holly, J. M. P., Perks, C. M. Tags: Research Source Type: research

Metformin alters H2A.Z dynamics and regulates androgen dependent prostate cancer progression.
Authors: Tyagi M, Cheema MS, Dryhurst D, Eskiw CH, Ausió J Abstract Epigenetic mechanisms involved in prostate cancer include hypermethylation of tumor suppressor genes, general hypomethylation of the genome, and alterations in histone posttranslational modifications (PTMs). In addition, over expression of the histone variant H2A.Z as well as deregulated expression of Polycomb group proteins including EZH2 have been well-documented. Recent evidence supports a role for metformin in prostate cancer (PCa) treatment. However, the mechanism of action of metformin in PCa is poorly understood. We provide data showing tha...
Source: Oncotarget - January 18, 2019 Category: Cancer & Oncology Tags: Oncotarget Source Type: research

Abstracts of Presentations at the Association of Clinical Scientists 143 < sup > rd < /sup > Meeting Louisville, KY May 11-14,2022
Conclusion: These assays are suitable for routine diagnostic. The UltraFast NextGenPCR is the fastest with average time (30mins), followed by Agilent (2 hrs) and MassArray (6hrs). Upon completion of this activity, participants should be able to examine, measure and compare results from different assays for SARS detection, evaluate and diagnose accurately, as well as being able to plan, organize and recommend a diagnostic procedure for diagnostic laboratory. Key words: SARS-CoV-2, RNA extraction, RT-PCR, limit of detection, quantification cycle, COVID-19, in vitro diagnostic tests, Agilent, Massarray, Ultrafast. [20] From t...
Source: Annals of Clinical and Laboratory Science - July 1, 2022 Category: Laboratory Medicine Source Type: research