ArticleEndocrine2022
Metformin exerts an antitumoral effect on papillary thyroid cancer cells through altered cell energy metabolism and sensitized by BACH1 depletion.
Article in Endocrine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Reprogramming of Thyroid Cancer Metabolism: from Mechanism to Therapeutic Strategy.Molecular cancer · 2025Review
- The Multifaceted Roles of BACH1 in Disease: Implications for Biological Functions and Therapeutic Applications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Metformin induces tumor immunogenic cell death in ovarian cancer by activating AMPK pathway.Translational oncology · 2024Article
- Metabolic Reprogramming in Thyroid Cancer.Endocrinology and metabolism (Seoul, Korea) · 2024Review
- Transcription factor BACH1 in cancer: roles, mechanisms, and prospects for targeted therapy.Biomarker research · 2024Review
- Toward Systems-Level Metabolic Analysis in Endocrine Disorders and Cancer.Endocrinology and metabolism (Seoul, Korea) · 2023Review
- Targeting Mitochondrial Metabolic Reprogramming as a Potential Approach for Cancer Therapy.International journal of molecular sciences · 2023Review
- The dual role and mutual dependence of heme/HO-1/Bach1 axis in the carcinogenic and anti-carcinogenic intersection.Journal of cancer research and clinical oncology · 2023Review
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeAberrant cell energy metabolism is one of the features of thyroid carcinogenesis. Metformin may reduce the risk of cancer, and BACH1 was reported to affect the sensitivity of cancer cells to metformin. The aims of this study were to investigate whether metformin exerts antitumor effects in PTC cells and explore the role of BACH1 depletion on the sensitivity of PTC cells to metformin.
methodsThe viability and proliferation of PTC cell lines were analyzed with MTT and colony forming assay. Energy utilization and mitochondrial respiration were measured using Seahorse XF instruments and Mitochondrial complex-1 activity assay.
resultsOur results showed the anti-proliferative and pro-apoptotic effects of metformin in PTC cells. Furthermore, metformin changed the pattern of cell energy metabolism in PTC cells, which manifested as inhibition of mitochondrial respiration, and the combination of BACH1 depletion with metformin magnified the effect of metformin alone.
conclusionsIn conclusion, metformin exerts an antitumoral effect on PTC cells both in vitro and in xenograft mouse models. A possible mechanism is through inhibiting glucose metabolism and mitochondrial respiration process. Knocking down BACH1 caused the switching of energy metabolism and sensitized PTC cells to metformin, which eventually enhanced the anti-tumor effect of metformin.
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