The association between metformin use and colorectal cancer survival among patients with diabetes mellitus: An updated meta‐analysis

Tian, Shan; Lei, Hongbo; Liu, Yulan; Chen, Yan; Dong, Weiguo

doi:10.1016/j.cdtm.2017.06.001

Cited by 11 publications

(18 citation statements)

References 41 publications

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“…As an oral drug controlling blood glucose in diabetes patients, metformin exerts an antiproliferative effect in multiple cancers including prostate cancer, lung cancer, colon cancer or breast cancer. 8,9 However, the function of metformin in preventing breast cancer growth and molecular regulatory mechanism is unclear and needs further clarification. We subsequently performed a cell viability analysis using breast cancer MCF-7 and BT-474 cell lines with or without the administration of metformin.…”

Section: Resultsmentioning

confidence: 99%

“…For the molecular mechanism of metformin in cancer treatment, it has been reported to inactivate STAT3 or NF‐κB, preventing IL‐6‐induced breast cancer progression . In prostate cancer, lung cancer, colon cancer or breast cancer patients with T2DM, metformin has been shown to reduce the development of tumor and prolong the survival . Metformin together with phenformin also resists the development of colon cancer through promoting AMPK and ROS production and inhibiting glycolysis .…”

Section: Discussionmentioning

confidence: 99%

“…7 In prostate cancer, lung cancer, colon cancer or breast cancer patients with T2DM, metformin has been shown to reduce the development of tumor and prolong the survival. 8,9 Metformin together with phenformin also resists the development of colon cancer through promoting AMPK and ROS production and inhibiting glycolysis. [15][16][17] In our study, we were interested in ascertaining the novel targets of metformin in cancer, especially in breast cancer.…”

Section: Discussionmentioning

confidence: 99%

“…Metformin is able to inactivate STAT3 and NF‐κB to suppress IL‐6‐induced breast cancer progression . Some researchers have observed that metformin can reduce the development of tumor and prolong the survival of patients with T2DM and different cancers, such as prostate cancer, lung cancer, colon cancer or breast cancer . In certain types of cancer including melanoma, ovarian, prostate, lung, colon or breast cancers, metformin and phenformin have been shown to prevent tumor progression .…”

Section: Introductionmentioning

confidence: 99%

“…7 Some researchers have observed that metformin can reduce the development of tumor and prolong the survival of patients with T2DM and different cancers, such as prostate cancer, lung cancer, colon cancer or breast cancer. 8,9 In certain types of cancer including melanoma, ovarian, prostate, lung, colon or breast cancers, metformin and phenformin have been shown to prevent tumor progression. [10][11][12][13][14] Metformin together with phenformin also play roles in resisting the development of colon cancer through promoting AMPK and ROS production and inhibiting glycolysis.…”

Section: Introductionmentioning

confidence: 99%

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Metformin alleviates breast cancer through targeting high‐mobility group AT‐hook 2

Wang

Ren

et al. 2020

Thoracic Cancer

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Background As a classic oral drug used in diabetic patients, metformin has exhibited an anticancer role in many types of cancers in recent years. Here, we aimed to investigate the role of metformin in the growth of breast cancer and its novel targets. Methods A cell viability assay was utilized to examine the inhibitory effect of metformin on proliferation of breast cancer cells. Western blotting and RT‐PCR assays were used to detect the regulation of metformin on the expression of oncogenic HMGA2. The luciferase reporter vector of HMGA2 promoter was constructed. A luciferase reporter gene assay was performed to analyze the effect of metformin on HMGA2 promoter activity in breast cancer cells. Chromatin immunoprecipitation (ChIP) assay was performed to show the binding of Sp1 to HMGA2 promoter in breast cancer cells with or without metformin treatment. The function of metformin‐regulated HMGA2 in breast cancer growth was tested using a cell viability assay. Results Cell proliferation was obviously inhibited in breast cancer cells treated with different concentrations of metformin. The level of mRNA and protein of HMGA2 was significantly reduced by metformin in the cells. Mechanistically, metformin was able to inactivate the HMGA2 promoter through downregulating transcription factor Sp1 in the cells. In terms of function, treatment with metformin suppressed the proliferation of breast cancer cells and overexpressed HMGA2 reversed the inhibition of cell proliferation mediated by metformin. Conclusion Metformin resists the growth of breast cancer through targeting Sp1/HMGA2 signal.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Metformin alleviates breast cancer through targeting high‐mobility group AT‐hook 2

Wang

Ren

et al. 2020

Thoracic Cancer

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Metformin treatment response is dependent on glucose growth conditions and metabolic phenotype in colorectal cancer cells

Alhourani

Tidwell

Bokil

et al. 2021

Sci Rep

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Cancer cells exhibit altered metabolism, a phenomenon described a century ago by Otto Warburg. However, metabolic drug targeting is considered an underutilized and poorly understood area of cancer therapy. Metformin, a metabolic drug commonly used to treat type 2 diabetes, has been associated with lower cancer incidence, although studies are inconclusive concerning effectiveness of the drug in treatment or cancer prevention. The aim of this study was to determine how glucose concentration influences cancer cells’ response to metformin, highlighting why metformin studies are inconsistent. We used two colorectal cancer cell lines with different growth rates and clinically achievable metformin concentrations. We found that fast growing SW948 are more glycolytic in terms of metabolism, while the slower growing SW1116 are reliant on mitochondrial respiration. Both cell lines show inhibitory growth after metformin treatment under physiological glucose conditions, but not in high glucose conditions. Furthermore, SW1116 converges with SW948 at a more glycolytic phenotype after metformin treatment. This metabolic shift is supported by changed GLUT1 expression. Thus, cells having different metabolic phenotypes, show a clear differential response to metformin treatment based on glucose concentration. This demonstrates the importance of growth conditions for experiments or clinical studies involving metabolic drugs such as metformin.

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Impact of metformin use on survival outcomes in non-small cell lung cancer treated with platinum

Xin

Xiao²,

Ding³

et al. 2018

Medicine

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Preclinical evidence suggests that metformin, a widely used antidiabetic drug, may have a sensitizing effect on platinum. The purpose of this study was to evaluate the survival outcomes for non-small cell lung cancer (NSCLC) patients with type 2 diabetes mellitus (T2DM) using metformin during platinum-based chemotherapy.The clinicopathological parameters and survival data of 75 NSCLC patients with T2DM from January 2008 to December 2011 were collected and analyzed retrospectively. Patients were divided into 2 groups: metformin exposure group (n = 27) and non-metformin group (patients using other hypoglycemic agents or no drug for controlling n = 48). Univariate and multivariate analyses were performed to assess the association of metformin usage with overall survival (OS).Mean follow-up time was 58.7 months. The mean survival time was 36.74 months in the metformin group and 40.21 months in the non-metformin group. There was no significant difference in survival time between the 2 groups (P = .661). After adjusting gender, age, smoking status, tumor stage, tumor histology, and differentiation, multivariate analysis showed that metformin was not associated with the OS in NSCLC patients treated with concurrent platinum-based chemotherapy (hazard ratio: 1.071, 95% confidence interval: 0.577–1.986, P = .828).Our results indicated that metformin exposure had no significant effect on OS in NSCLC patients treated with platinum-based chemotherapy. Further studies are warranted to evaluate whether metformin could affect the survival of NSCLC patients treated with platinum-based chemotherapy.

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The association between metformin use and colorectal cancer survival among patients with diabetes mellitus: An updated meta‐analysis

Cited by 11 publications

References 41 publications

Metformin alleviates breast cancer through targeting high‐mobility group AT‐hook 2

Metformin alleviates breast cancer through targeting high‐mobility group AT‐hook 2

Metformin treatment response is dependent on glucose growth conditions and metabolic phenotype in colorectal cancer cells

Impact of metformin use on survival outcomes in non-small cell lung cancer treated with platinum

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