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Drug: Metformin

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Total 6513 results found since Jan 2013.

Metformin Relieves Bortezomib-Induced Neuropathic Pain by Regulating AMPKa2-Mediated Autophagy in the Spinal Dorsal Horn
Neurochem Res. 2022 Mar 12. doi: 10.1007/s11064-022-03571-7. Online ahead of print.ABSTRACTChemotherapy-induced neuropathic pain is a major clinical problem with limited treatment options. Here, we show that metformin relieves bortezomib (BTZ)-evoked induction and maintenance of neuropathic pain by preventing the reduction in the expression of Beclin-1, an autophagy marker, in the spinal dorsal horn. Application of rapamycin or 3-methyladenine, autophagy inducer and inhibitor, respectively, affected the mechanical allodynia differently. Co-application of 3-methyladenine and metformin partially inhibited the effect of metfo...
Source: Neurochemical Research - March 12, 2022 Category: Neuroscience Authors: Meng Liu Yu-Ting Zhao You-You Lv Ting Xu Dai Li Yuan-Chang Xiong Wen-Jun Xin Su-Yan Lin Source Type: research

Reversal of multidrug resistance of hepatocellular carcinoma cells by metformin through inhibiting NF- κB gene transcription.
CONCLUSION: Metformin via silencing NF-κB signaling could effectively reverse MDR of HCC cells by down-regulating MDR1/P-gp expression. PMID: 27621764 [PubMed]
Source: World Journal of Hepatology - September 15, 2016 Category: Gastroenterology Tags: World J Hepatol 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

Metformin Improves the Senescence of Renal Tubular Epithelial Cells in a High-Glucose State Through E2F1
In this study, we explored whether metformin improves a high-glucose-induced senescence and fibrosis of renal tubular epithelial cells through cell cycle-related protein E2F1. In the in vivo experiments, the recombinant adeno-associated virus (AAV-shE2F1) knockdown E2F1 gene was injected into the tail vein of 16-weeks-old db/db mice for 8 weeks. The 16-week-old db/db mice were administered metformin (260 mg/kg/d) continuously for 8 weeks. The normal control group (NC) and diabetic model group (DM) were set up simultaneously. Mice renal tubular epithelial cells (mRTECs) were cultured in vitro. The cells were randomly div...
Source: Frontiers in Pharmacology - June 23, 2022 Category: Drugs & Pharmacology Source Type: research

Metformin Suppresses Hepatocellular Carcinoma through Regulating Alternative Splicing of LGR4
CONCLUSIONS: LGR4 could promote the ability of cell proliferation, migration, and invasion in HCC, which could be reduced by metformin through alternative splicing.PMID:36385965 | PMC:PMC9652085 | DOI:10.1155/2022/1774095
Source: Journal of Oncology - November 17, 2022 Category: Cancer & Oncology Authors: Han Zhuo Shuying Miao Zhenquan Jin Deming Zhu Zhenggang Xu Dongwei Sun Jie Ji Zhongming Tan Source Type: research

Metformin-mediated downregulation of p38 mitogen-activated protein kinase-dependent excision repair cross-complementing 1 decreases DNA repair capacity and sensitizes human lung cancer cells to paclitaxel.
Abstract Metformin, an extensively used and well-tolerated drug for treating individuals with type 2 diabetes, has recently gained significant attention as an anticancer drug. On the other hand, paclitaxel (Taxol) is a new antineoplastic drug that has shown promise in the treatment of non-small cell lung cancer (NSCLC). High expression levels of excision repair cross-complementary 1 (ERCC1) in cancers have been positively associated with the DNA repair capacity and a poor prognosis in NSCLC patients treated with platinum-containing chemotherapy. In this current study, paclitaxel was found to increase phosphorylati...
Source: Biochemical Pharmacology - December 7, 2012 Category: Drugs & Pharmacology Authors: Tseng SC, Huang YC, Chen HJ, Chiu HC, Huang YJ, Wo TY, Weng SH, Lin YW Tags: Biochem Pharmacol Source Type: research

Regulation of metformin response by breast cancer associated gene 2.
Abstract Adenosine monophosphate-activated protein kinase (AMPK), a master regulator of cellular energy homeostasis, has emerged as a promising molecular target in the prevention of breast cancer. Clinical trials using the United States Food and Drug Administration (FDA)-approved, AMPK-activating, antidiabetic drug metformin are promising in this regard, but the question of why metformin is protective for some women but not others still remains. Breast cancer associated gene 2 (BCA2/Rabring7/RNF115), a novel Really Interesting New Gene (RING) finger ubiquitin E3 ligase, is overexpressed in >50% of breast tumors...
Source: Neoplasia - December 1, 2013 Category: Cancer & Oncology Authors: Buac D, Kona FR, Seth AK, Dou QP Tags: Neoplasia Source Type: research

Metformin induces PGC‐1α expression and selectively affects hepatic PGC‐1α functions
Conclusions and ImplicationsDownregulation of PGC‐1α is not necessary for suppression of gluconeogenic genes by metformin. Importantly, metformin selectively regulates hepatic PGC‐1α‐mediated gene regulation and prevents activation of gluconeogenesis, but leaves regulation of mitochondrial genes intact. Our results thus identify selective modulation of hepatic PGC‐1α functions as a novel mechanism involved in the therapeutic action of metformin.
Source: British Journal of Pharmacology - January 16, 2014 Category: Drugs & Pharmacology Authors: Sanna‐Mari Aatsinki, Marcin Buler, Henriikka Salomäki, Markku Koulu, Petr Pavek, Jukka Hakkola Tags: Research Paper Source Type: research

Involvement of the AMPK-PTEN pathway in insulin resistance induced by high glucose in cultured rat podocytes.
Abstract As part of the filtration barrier, podocytes play an important role in the development of diabetic nephropathy. Disturbances in insulin signaling accompanied by insulin resistance can lead to various intracellular events. We hypothesized that high glucose concentrations would lead to disturbances in interactions between AMPK and PTEN proteins in podocytes. Experiments were performed in primary rat podocytes cultured with normal (5.6mM) or high (30mM) glucose concentrations for 5 d. Immunodetection methods were used to detect AMPK, PTEN, insulin receptor, and Akt proteins, and their phosphorylated forms. I...
Source: The International Journal of Biochemistry and Cell Biology - April 15, 2014 Category: Biochemistry Authors: Rogacka D, Piwkowska A, Audzeyenka I, Angielski S, Jankowski M Tags: Int J Biochem Cell Biol Source Type: research

Repression of phosphoinositide-dependent protein kinase 1 expression by ciglitazone via Egr-1 represents a new approach for inhibition of lung cancer cell growth
Conclusion: Collectively, our results demonstrate that ciglitazone inhibits PDK1 expression through AMPKalpha-mediated induction of Egr-1 and Egr-1 binding to the specific DNA site in the PDK1 gene promoter, which is independent of PPARgamma. Activation of AMPKalpha by metformin enhances the effect of ciglitazone. In turn, this leads to inhibition of NSCLC cell proliferation.
Source: Epidemiologic Perspectives and Innovations - June 13, 2014 Category: Epidemiology Authors: SWei Sunny HannQing TangFang ZhengShunyu ZhaoJianping ChenZhiYu Wang Source Type: research

Activation of AMP-activated protein kinase inhibits ER stress and renal fibrosis.
In conclusion, AMPK may serve as a promising therapeutic target through reducing ER stress and renal fibrosis. PMID: 25428127 [PubMed - as supplied by publisher]
Source: American Journal of Physiology. Renal Physiology - November 26, 2014 Category: Physiology Authors: Kim H, Moon SY, Kim JS, Baek CH, Kim M, Min JY, Lee SK Tags: Am J Physiol Renal Physiol Source Type: research

Impact of AMPK on Glucosylceramide Metabolism Glycobiology and Extracellular Matrices
The membrane glycolipid glucosylceramide (GlcCer) plays a critical role in cellular homeostasis. Its intracellular levels are thought to be tightly regulated. How cells regulate GlcCer levels remains to be clarified. AMP-activated protein kinase (AMPK), which is a crucial cellular energy sensor, regulates glucose and lipid metabolism to maintain energy homeostasis. Here, we investigated whether AMPK affects GlcCer metabolism. AMPK activators (5-aminoimidazole-4-carboxamide 1-β-d-ribofuranoside and metformin) decreased intracellular GlcCer levels and synthase activity in mouse fibroblasts. AMPK inhibitors or AMPK siRNA rev...
Source: Journal of Biological Chemistry - July 16, 2015 Category: Chemistry Authors: Ishibashi, Y., Hirabayashi, Y. Tags: Lipids Source Type: research

Metformin inhibits growth of human non-small cell lung cancer cells via liver kinase B-1-independent activation of adenosine monophosphate-activated protein kinase.
Authors: Guo Q, Liu Z, Jiang L, Liu M, Ma J, Yang C, Han L, Nan K, Liang X Abstract Metformin, the most widely administered oral anti‑diabetic therapeutic agent, exerts its glucose-lowering effect predominantly via liver kinase B1 (LKB1)-dependent activation of adenosine monophosphate-activated protein kinase (AMPK). Accumulating evidence has demonstrated that metformin possesses potential antitumor effects. However, whether the antitumor effect of metformin is via the LKB1/AMPK signaling pathway remains to be determined. In the current study, the effects of metformin on proliferation, cell cycle progression, and...
Source: Molecular Medicine Reports - February 9, 2016 Category: Molecular Biology Tags: Mol Med Rep Source Type: research

The roles of tricellular tight junction protein lipolysis-stimulated lipoprotein receptor in malignancy of human endometrial cancer cells.
Authors: Shimada H, Satohisa S, Kohno T, Takahashi S, Hatakeyama T, Konno T, Tsujiwaki M, Saito T, Kojima T Abstract Lipolysis-stimulated lipoprotein receptor (LSR) has been identified as a novel molecular constituent of tricellular contacts that have a barrier function for the cellular sheet. LSR recruits tricellulin (TRIC), which is the first molecular component of tricellular tight junctions. Knockdown of LSR increases cell motility and invasion of certain cancer cells. However, the behavior and the roles of LSR in endometrial cancer remain unknown. In the present study, we investigated the behavior and roles of...
Source: Oncotarget - April 3, 2016 Category: Cancer & Oncology Tags: Oncotarget Source Type: research