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Metformin and synergism

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https://www.readbyqxmd.com/read/30251898/metformin-and-its-sulphonamide-derivative-simultaneously-potentiateanti-cholinesterase-activity-of-donepezil-and-inhibit-beta-amyloid-aggregation
#1
Magdalena Markowicz-Piasecka, Kristiina M Huttunen, Joanna Sikora
The aim of this study was to assess in vitro the effects of sulphenamide and sulphonamide derivatives of metformin on the activity of human acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE), establish the type of inhibition, and assess the potential synergism between biguanides and donepezil towards both cholinesterases (ChEs) and the effects on the β-amyloid aggregation. Sulphonamide 5 with para-trifluoromethyl- and ortho-nitro substituents in aromatic ring inhibited AChE in a mixed-type manner at micromolar concentrations (IC50  = 212...
December 2018: Journal of Enzyme Inhibition and Medicinal Chemistry
https://www.readbyqxmd.com/read/30149143/metformin-enhances-cisplatin-induced-apoptosis-and-prevents-resistance-to-cisplatin-in-co-mutated-kras-lkb1-non-small-cell-lung-cancer-nsclc
#2
Massimo Moro, Elisa Caiola, Monica Ganzinelli, Elisabetta Zulato, Eliana Rulli, Mirko Marabese, Giovanni Centonze, Adele Busico, Ugo Pastorino, Filippo G de Braud, Claudio Vernieri, Michele Simbolo, Emilio Bria, Aldo Scarpa, Stefano Indraccolo, Massimo Broggini, Gabriella Sozzi, Marina Chiara Garassino
PURPOSE: we hypothesized that activating KRAS mutations and inactivation of the LKB1 oncosuppressor can cooperate to sustain NSCLC aggressiveness. We also hypothesized that the growth advantage of KRAS/LKB1 co-mutated tumors could be balanced by higher sensitivity to metabolic stress conditions, such as metformin treatment, thus revealing new strategies to target this aggressive NSCLC subtype. EXPERIMENTAL DESIGN: we retrospectively determined the frequency and prognostic value of KRAS/LKB1 co-mutations in tissue specimens from NSCLC patients enrolled in the TAILOR trial...
August 24, 2018: Journal of Thoracic Oncology
https://www.readbyqxmd.com/read/30030256/sglt2-inhibitors-in-combination-therapy-from-mechanisms-to-clinical-considerations-in-type-2-diabetes-management
#3
REVIEW
Michaël J B van Baar, Charlotte C van Ruiten, Marcel H A Muskiet, Liselotte van Bloemendaal, Richard G IJzerman, Daniël H van Raalte
The progressive nature of type 2 diabetes (T2D) requires practitioners to periodically evaluate patients and intensify glucose-lowering treatment once glycemic targets are not attained. With guidelines moving away from a one-size-fits-all approach toward setting patient-centered goals and allowing flexibility in choosing a second-/third-line drug from the growing number of U.S. Food and Drug Administration-approved glucose-lowering agents, keen personalized management in T2D has become a challenge for health care providers in daily practice...
August 2018: Diabetes Care
https://www.readbyqxmd.com/read/30023463/combination-of-bez235-and-metformin-has-synergistic-effect-on-cell-viability-in-colorectal-cancer-cells
#4
Taewan Kim, Taehyung Kim, Soonyoung Choi, Hyeran Ko, Deokbae Park, Youngki Lee
Patients with type II diabetes mellitus are more susceptible to colorectal cancer (CRC) incidence than non-diabetics. The anti-diabetic drug metformin is most commonly prescribed for the treatment of this disease and has recently shown antitumor effect in preclinical studies. The aberrant mutational activation in the components of RAS/RAF/MEK/ERK and PI3K/AKT/mTOR signaling pathway is very frequently observed in CRC. We previously reported that metformin inhibits the phosphorylation of ERK and BEZ235, a dual inhibitor of PI3K and mTOR, has anti-tumor activity against HCT15 CRC cells harboring mutations of KRAS and PIK3CA...
June 2018: Balsaeng'gwa Saengsig
https://www.readbyqxmd.com/read/29865997/combination-of-sglt-2-inhibitors-and-glp-1-receptor-agonists-potential-benefits-in-surrogate-and-hard-endpoints
#5
Michael Doumas, Κonstantinos Imprialos, Konstantinos Stavropoulos, Andromachi Reklou, Alexandros Sachinidis, Vasilios G Athyros
BACKGROUND: The treatment of type 2 diabetes mellitus (T2DM) is complex; only a few patients successfully attain glycemic targets with monotherapy, most requiring drug combination therapy. METHODS: The goal of this review was to identify in PubMed the complimentary ways of action leading to clinical benefit (in lowering HbA1c, body weight, renal, and cardiac risk factors and events) of the combination of sodium glucose cotransporter 2 inhibitors (SGLT2i) and glucagon-like peptide-1 receptor agonists (GLP-1 RA)...
2018: Current Pharmaceutical Design
https://www.readbyqxmd.com/read/29434877/metformin-synergizes-with-rapamycin-to-inhibit-the-growth-of-pancreatic-cancer-in-vitro-and-in-vivo
#6
Jia-Wei Zhang, Fan Zhao, Qing Sun
Previous studies have suggested that metformin may improve the survival rate of patients with pancreatic cancer (PC) by regulating the adenosine monophosphate-activated protein kinase/mammalian target of rapamycin (mTOR) signaling pathway. Rapamycin specifically targets mTOR. In the present study, the efficacy of metformin and rapamycin in isolation and combination were investigated for the treatment of PC. The efficacy of metformin and rapamycin in reducing the proliferation of PC cell line SW1990 in vitro and in vivo was evaluated...
February 2018: Oncology Letters
https://www.readbyqxmd.com/read/29396233/in-vivo-evaluation-of-the-synergic-effect-of-metformin-and-mtor-inhibitors-on-the-endothelial-healing-of-drug-eluting-stents-in-diabetic-patients
#7
Héctor Cubero-Gallego, Rafael Romaguera, Josep Gómez-Lara, Joan A Gómez-Hospital, Manel Sabaté, Eduardo Pinar, Montserrat Gracida, Gerard Roura, José L Ferreiro, Luis Teruel, Cristian Tebé-Codorni, Pilar Jiménez-Quevedo, Eduard Montanya, Fernando Alfonso, Ángel Cequier
INTRODUCTION AND OBJECTIVES: Recent animal studies have shown metformin (MF) to impair endothelialization of drug-eluting stents (DES). The aim of this study was to evaluate the effect of MF on the healing of DES in human coronary arteries of patients with diabetes mellitus by optical coherence tomography (OCT). METHODS: The RESERVOIR trial randomized 116 lesions in 112 patients with diabetes mellitus to amphilimus- or everolimus-eluting stents and included mandatory OCT at 9 months of follow-up...
January 25, 2018: Revista Española de Cardiología
https://www.readbyqxmd.com/read/29386513/hexokinase-2-depletion-inhibits-glycolysis-and-induces-oxidative-phosphorylation-in-hepatocellular-carcinoma-and-sensitizes-to-metformin
#8
Dannielle DeWaal, Veronique Nogueira, Alexander R Terry, Krushna C Patra, Sang-Min Jeon, Grace Guzman, Jennifer Au, Christopher P Long, Maciek R Antoniewicz, Nissim Hay
Hepatocellular carcinoma (HCC) cells are metabolically distinct from normal hepatocytes by expressing the high-affinity hexokinase (HK2) and suppressing glucokinase (GCK). This is exploited to selectively target HCC. Hepatic HK2 deletion inhibits tumor incidence in a mouse model of hepatocarcinogenesis. Silencing HK2 in human HCC cells inhibits tumorigenesis and increases cell death, which cannot be restored by GCK or mitochondrial binding deficient HK2. Upon HK2 silencing, glucose flux to pyruvate and lactate is inhibited, but TCA fluxes are maintained...
January 31, 2018: Nature Communications
https://www.readbyqxmd.com/read/29348889/metformin-and-temozolomide-a-synergic-option-to-overcome-resistance-in-glioblastoma-multiforme-models
#9
Silvia Valtorta, Alessia Lo Dico, Isabella Raccagni, Daniela Gaglio, Sara Belloli, Letterio S Politi, Cristina Martelli, Cecilia Diceglie, Marcella Bonanomi, Giulia Ercoli, Valentina Vaira, Luisa Ottobrini, Rosa Maria Moresco
Glioblastoma multiforme (GBM) is the most aggressive primary brain tumor with poor survival. Cytoreduction in association with radiotherapy and temozolomide (TMZ) is the standard therapy, but response is heterogeneous and life expectancy is limited. The combined use of chemotherapeutic agents with drugs targeting cell metabolism is becoming an interesting therapeutic option for cancer treatment. Here, we found that metformin (MET) enhances TMZ effect on TMZ-sensitive cell line (U251) and overcomes TMZ-resistance in T98G GBM cell line...
December 22, 2017: Oncotarget
https://www.readbyqxmd.com/read/29227654/synergistic-chemopreventive-and-therapeutic-effects-of-co-drug-ua-met-implication-in-tumor-metastasis
#10
Guirong Zheng, Zhichun Shen, Aixiao Xu, Kai Jiang, Pengyu Wu, Xiang Yang, Xian Chen, Jingwei Shao
The anticancer properties of ursolic acid (UA) and metformin (Met) have been well demonstrated. However, whether these compounds can act synergistically to prevent and treat cancer is not known. We present in this study, the synergism between UA and Met, and that of a new codrug made of UA and Met (UA-Met) against several cancer cell lines. The combination of high concentration of UA (25, 50, 75, 100 μM) and Met (5, 10, 20, 40 mM) resulted in synergetic cytotoxicity on MDA-MB-231 and MCF-7 cells (CI < 0...
December 20, 2017: Journal of Agricultural and Food Chemistry
https://www.readbyqxmd.com/read/28618116/differences-in-p53-status-significantly-influence-the-cellular-response-and-cell-survival-to-1-25-dihydroxyvitamin-d3-metformin-cotreatment-in-colorectal-cancer-cells
#11
Mohamed A Abu El Maaty, Wendy Strassburger, Tooba Qaiser, Yasamin Dabiri, Stefan Wölfl
Mutations in the tumor suppressor p53 are highly prevalent in cancers and are known to influence the sensitivity of cells to various chemotherapeutics including the anti-cancer candidates 1,25-dihydrovitamin D3 [1,25D3] and metformin. Previous studies have demonstrated additive/synergistic anti-cancer effects of the 1,25D3-metformin combination in different models, however, the influence of p53 status on the efficacy of this regimen has not been investigated. The CRC colorectal cancer (CRC) cell lines HCT116 wild-type (wt), HCT116 p53-/-, and HT-29 (mutant; R273H) were employed, covering three different p53 variations...
November 2017: Molecular Carcinogenesis
https://www.readbyqxmd.com/read/28576465/metformin-and-caffeic-acid-regulate-metabolic-reprogramming-in-human-cervical-carcinoma-siha-htb-35-cells-and-augment-anticancer-activity-of-cisplatin-via-cell-cycle-regulation
#12
Malgorzata Tyszka-Czochara, Karolina Bukowska-Strakova, Marcin Majka
Metformin shows benefits in anticancer prevention in humans. In this study, normal human fibroblasts (FB) and metastatic cervical cancer cells (SiHa) were exposed to 10 mM Metformin (Met), 100 μM Caffeic Acid (trans-3,4-dihydroxycinnamic acid, CA) or combination of the compounds. Both drugs were selectively toxic towards cancer cells, but neither Met nor CA treatment suppressed growth of normal cells. Met and CA regulated metabolic reprogramming in SiHa tumor cells through different mechanisms: Met suppressed regulatory enzymes Glurtaminase (GLS) and Malic Enzyme 1 (ME1) and enhanced pyruvate oxidation via tricarboxylic acids (TCA) cycle, while CA acted as glycolytic inhibitor...
August 2017: Food and Chemical Toxicology
https://www.readbyqxmd.com/read/28545687/synergistic-effect-of-mek-inhibitor-and-metformin-combination-in-low-grade-serous-ovarian-cancer
#13
Ismail Mert, Jasdeep Chhina, Ghassan Allo, Jing Dai, Shelly Seward, Mark S Carey, Marta Llaurado, Shailendra Giri, Ramandeep Rattan, Adnan R Munkarah
OBJECTIVE: Low-grade serous ovarian cancer (LGSOC) constitutes 5-8% of epithelial ovarian cancers and is refractory to chemotherapy. We and others have shown metformin to cause significant growth inhibition in high-grade ovarian cancer both in vitro and in vivo. Here, we aimed to analyze if metformin was effective in inhibiting proliferation of LGSOC alone and in combination with MEK inhibitor. METHODS: Three LGSOC lines (VOA1056, VOA1312 and VOA5646) were treated with metformin, trametinib or 2-deoxyglucose (2DG) alone or in combination with metformin...
August 2017: Gynecologic Oncology
https://www.readbyqxmd.com/read/28533436/metformin-synergizes-with-bcl-xl-bcl-2-inhibitor-abt-263-to-induce-apoptosis-specifically-in-p53-defective-cancer-cells
#14
Xinzhe Li, Bo Li, Zhenhong Ni, Peng Zhou, Bin Wang, Jintao He, Haojun Xiong, Fan Yang, Yaran Wu, Xilin Lyu, Yan Zhang, Yijun Zeng, Jiqin Lian, Fengtian He
p53 deficiency, a frequent event in multiple kinds of malignancies, decreases the sensitivity of diverse targeted chemotherapeutics including the BCL-XL/BCL-2 inhibitor ABT-263. Loss of p53 function can activate mTOR complex 1 (mTORC1), which may make it a vulnerable target. Metformin has shown anti-neoplastic efficiency partially through suppressing mTORC1. However, it remains unknown whether mTORC1 activation confers ABT-263 resistance and whether metformin can overcome it in the p53-defective contexts. In this study, we for the first time demonstrated that metformin and ABT-263 synergistically elicited remarkable apoptosis through orchestrating the proapoptotic machineries in various p53-defective cancer cells...
September 2017: Molecular Cancer Therapeutics
https://www.readbyqxmd.com/read/28529553/progress-in-the-application-and-mechanism-of-metformin-in-treating-non-small-cell-lung-cancer
#15
Chan Li, Yang Xue, Yu-Rong Xi, Ke Xie
At present, the incidence and mortality of lung cancer demonstrate an increasing trend. Non-small cell lung cancer (NSCLC) accounts for ~80-85% of all lung cancer cases. Therefore, developing novel and more effective treatments is of great importance. The use of combination therapies, where several anticancer agents are used together, is a promising strategy. Recent studies demonstrate that metformin, which has been utilized for treating diabetes mellitus for >50 years, has antitumor effects in numerous types of cancer including NSCLC...
May 2017: Oncology Letters
https://www.readbyqxmd.com/read/28480372/free-fatty-acids-profiling-in-response-to-carnitine-synergize-with-lutein-in-diabetic-rats
#16
Abdulrahman L Al-Malki, Said S Moselhy
BACKGROUND: The objective of this study was to investigate the fatty acids profiling in diabetic rats induced by sterptozocine (STZ) and their response to administration of lutein and carnitine. MATERIALS AND METHODS: Ninety male albino rats were divided into 6 groups as follows: Normal control. The remaining rats were injected i.p a single dose of STZ (65 mg /kg bw) for induction of diabetes. Diabetic rats were grouped as: GP II: (Untreated): GP III: Rats were given orally with L-lutein (100 mg/kg bw)...
2016: African Journal of Traditional, Complementary, and Alternative Medicines: AJTCAM
https://www.readbyqxmd.com/read/28432330/enhanced-response-of-metformin-towards-the-cancer-cells-due-to-synergism-with-multi-walled-carbon-nanotubes-in-photothermal-therapy
#17
Sweejiang Yoo, Jin Hou, Wenhui Yi, Yingchun Li, Weiping Chen, Lingjie Meng, Jinhai Si, Xun Hou
Converging evidence from laboratory models pointed that the widely used antidiabetic drug metformin has direct effects on cancer cells. Thus far, relatively little attention has been addressed to the drug exposures used experimentally relative to those achievable clinically. Here, we demonstrated that metformin loaded on carbon nanotubes under near-infrared (NIR) irradiation led to the remarkably enhancement in response towards cancer cells. The dose of metformin has reduced to only 1/280 of typical doses in monotherapy (35: 10 000-30 000 µM) where the realization of metformin in conventional antidiabetic doses for cancer therapies becomes possible...
April 21, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28350075/co-treatment-of-breast-cancer-cells-with-pharmacologic-doses-of-2-deoxy-d-glucose-and-metformin-starving-tumors
#18
Ulrike Wokoun, Martin Hellriegel, Günter Emons, Carsten Gründker
A characteristic of tumor cells is the increased aerobic glycolysis for energy production. Thus, inhibition of glycolysis represents a selective therapeutic option. It has been shown that glycolysis inhibitor 2-deoxy-D-glucose (2DG) induces apoptotic cell death in different tumor entities. In addition, the antitumor activity of the anti-diabetic drug metformin has been demonstrated. In the present study, we aimed to ascertain whether the combination of pharmacologic doses of 2DG with metformin increases the antitumor efficacy...
April 2017: Oncology Reports
https://www.readbyqxmd.com/read/28230778/caffeic-acid-expands-anti-tumor-effect-of-metformin-in-human-metastatic-cervical-carcinoma-htb-34-cells-implications-of-ampk-activation-and-impairment-of-fatty-acids-de-novo-biosynthesis
#19
Malgorzata Tyszka-Czochara, Pawel Konieczny, Marcin Majka
The efficacy of cancer treatments is often limited and associated with substantial toxicity. Appropriate combination of drug targeting specific mechanisms may regulate metabolism of tumor cells to reduce cancer cell growth and to improve survival. Therefore, we investigated the effects of anti-diabetic drug Metformin (Met) and a natural compound caffeic acid ( trans -3,4-dihydroxycinnamic acid, CA) alone and in combination to treat an aggressive metastatic human cervical HTB-34 (ATCC CRL-1550) cancer cell line...
February 21, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28208838/the-effect-of-metformin-and-gant61-combinations-on-the-radiosensitivity-of-prostate-cancer-cells
#20
Annelies Gonnissen, Sofie Isebaert, Chad M McKee, Ruth J Muschel, Karin Haustermans
The anti-diabetes drug metformin has been shown to have anti-neoplastic effects in several tumor models through its effects on energy metabolism and protein synthesis. Recent studies show that metformin also targets Hedgehog (Hh) signaling, a developmental pathway re-activated in several tumor types, including prostate cancer (PCa). Furthermore, we and others have shown that Hh signaling is an important target for radiosensitization. Here, we evaluated the combination of metformin and the Hh inhibitor GANT61 (GLI-ANTagonist 61) with or without ionizing radiation in three PCa cell lines (PC3, DU145, 22Rv1)...
February 13, 2017: International Journal of Molecular Sciences
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