Mini Review - (2024) Volume 9, Issue 1
Received: 19-Jan-2024, Manuscript No. jdcm-24-129729;
Editor assigned: 22-Jan-2024, Pre QC No. P-129729;
Reviewed: 05-Feb-2024, QC No. Q-129729;
Revised: 10-Feb-2024, Manuscript No. R-129729;
Published:
17-Feb-2024
, DOI: 10.37421/2475-3211.2024.9.247
Citation: Benny, Daniel. “Metformin in Esophageal Carcinoma: Exploring Molecular Mechanisms and Therapeutic Insights.” J Diabetic Complications Med 9 (2024): 247.
Copyright: © 2024 Benny D. This is an open-access article distributed under the terms of the creative commons attribution license which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited.
Esophageal carcinoma is a challenging malignancy with limited treatment options and poor prognosis, necessitating the exploration of novel therapeutic strategies. Metformin, a widely used drug for type 2 diabetes, has shown promising anticancer effects in various malignancies, including esophageal carcinoma. This article provides an overview of the molecular mechanisms underlying the anticancer properties of metformin in esophageal carcinoma and discusses its therapeutic potential.
Metformin • Esophageal carcinoma • Molecular mechanisms • Therapeutic insights
Esophageal carcinoma ranks among the deadliest cancers worldwide, characterized by its aggressive nature, limited treatment options and poor prognosis. Despite advancements in therapy, the overall survival rates for esophageal carcinoma remain low, highlighting the urgent need for innovative treatment approaches. Metformin, an oral hypoglycemic agent, has garnered attention for its potential anticancer effects [1]. In this article, we delve into the molecular mechanisms through which metformin exerts its anticancer activity in esophageal carcinoma and explore its therapeutic implications.
Metformin activates AMPK, a key cellular energy sensor, leading to inhibition of mTOR signaling pathway. AMPK activation by metformin suppresses cell proliferation, induces cell cycle arrest and promotes apoptosis in esophageal carcinoma cells. Metformin disrupts cancer cell metabolism by inhibiting mitochondrial complex I, leading to decreased ATP production and altered cellular metabolism [2]. This metabolic reprogramming attenuates cancer cell growth and survival in esophageal carcinoma. Metformin inhibits the insulin/IGF signaling pathway, which is implicated in tumorigenesis and cancer progression. Suppression of IGF signaling by metformin impedes proliferation, migration and invasion of esophageal carcinoma cells [3,4].
By inhibiting EMT, metformin impedes invasion and metastasis of esophageal carcinoma cells, enhancing treatment efficacy. Metformin holds promise as an adjuvant therapy in esophageal carcinoma, complementing standard treatment modalities such as surgery, chemotherapy and radiotherapy. Clinical trials evaluating the efficacy of metformin as an adjuvant therapy in esophageal carcinoma are underway, with preliminary results showing encouraging outcomes. Combining metformin with conventional chemotherapeutic agents or targeted therapies may enhance treatment efficacy and overcome resistance mechanisms [5]. Synergistic interactions between metformin and other anticancer agents have been observed in preclinical studies, underscoring the potential for combination therapy in esophageal carcinoma. Identification of biomarkers predictive of metformin response can facilitate personalized treatment approaches in esophageal carcinoma. Biomarker-guided selection of patients likely to benefit from metformin therapy may optimize treatment outcomes and minimize unnecessary side effects [6].
Metformin emerges as a promising therapeutic agent for esophageal carcinoma, exerting anticancer effects through multiple molecular mechanisms. Its ability to target various hallmarks of cancer, including dysregulated metabolism, proliferative signaling and inflammation, underscores its potential as a multifaceted anticancer agent. Further research, including well-designed clinical trials, is warranted to elucidate the therapeutic efficacy and safety profile of metformin in the management of esophageal carcinoma.
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Journal of Diabetic Complications & Medicine received 102 citations as per Google Scholar report