Metformin exerts an antitumoral effect on papillary thyroid cancer cells through altered cell energy metabolism and sensitized by BACH1 depletion

Yu, Yang; Chen, Feng; Kuang, Jian; Guo, Lixin; Wang, Zhihong

doi:10.1007/s12020-021-02977-7

Cited by 11 publications

(3 citation statements)

References 48 publications

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“…Past study reported that Met reduced lung metastasis and improved chemotherapy sensitivity of liver cancer cells by inducing vessel normalization [ 30 ]. Also, Met could inhibit mitochondrial respiration to repress cell proliferation and promote apoptosis in papillary thyroid cancer [ 31 ]. Importantly, Met had been confirmed to overcome immunosuppression in colorectal cancer by enhancing CD8 + T cell cytotoxicity [ 32 ].…”

Section: Discussionmentioning

confidence: 99%

Metformin induces tumor immunogenic cell death in ovarian cancer by activating AMPK pathway

Chen,

Wang,

Chen

et al. 2024

Translational Oncology

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Section: Discussionmentioning

confidence: 99%

Metformin induces tumor immunogenic cell death in ovarian cancer by activating AMPK pathway

Chen,

Wang,

Chen

et al. 2024

Translational Oncology

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“…In addition, regulation of mitochondrial metabolism inhibits tumor growth by targeting BACH1, thereby sensitizing tumors to mitochondrial inhibitors. Hemin sensitizes TNBC to metformin by promoting the degradation of BACH1, making combined hemin-metformin treatment a potential therapeutic strategy for other cancer types, such as papillary thyroid carcinoma [ 10 , 154 ]. Targeted inhibition of HO-1 promotes the FBXO22-dependent degradation of BACH1, thereby reducing cell migration and metastasis, which has been demonstrated in animal models.…”

Section: Bach1 As a Therapeutic Targetmentioning

confidence: 99%

Transcription factor BACH1 in cancer: roles, mechanisms, and prospects for targeted therapy

Hu,

Zhang,

Luo

et al. 2024

Biomark Res

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Transcription factor BTB domain and CNC homology 1 (BACH1) belongs to the Cap ‘n’ Collar and basic region Leucine Zipper (CNC-bZIP) family. BACH1 is widely expressed in mammalian tissues, where it regulates epigenetic modifications, heme homeostasis, and oxidative stress. Additionally, it is involved in immune system development. More importantly, BACH1 is highly expressed in and plays a key role in numerous malignant tumors, affecting cellular metabolism, tumor invasion and metastasis, proliferation, different cell death pathways, drug resistance, and the tumor microenvironment. However, few articles systematically summarized the roles of BACH1 in cancer. This review aims to highlight the research status of BACH1 in malignant tumor behaviors, and summarize its role in immune regulation in cancer. Moreover, this review focuses on the potential of BACH1 as a novel therapeutic target and prognostic biomarker. Notably, the mechanisms underlying the roles of BACH1 in ferroptosis, oxidative stress and tumor microenvironment remain to be explored. BACH1 has a dual impact on cancer, which affects the accuracy and efficiency of targeted drug delivery. Finally, the promising directions of future BACH1 research are prospected. A systematical and clear understanding of BACH1 would undoubtedly take us one step closer to facilitating its translation from basic research into the clinic.

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“…A recent study investigated metabolic reprogramming in papillary thyroid cancer in vitro and in vivo when treated with metformin. Using an extracellular flux analyzer, metformin was shown to decrease mitochondrial respiration, respiration capacity, aerobic glycolysis, glycolytic capacity, and adenosine triphosphate production [ 44 ]. Metabolomics has also elucidated the mechanisms underlying metabolic alterations in different subtypes of thyroid cancer.…”

Section: Metabolism In Thyroid and Other Cancersmentioning

confidence: 99%

Toward Systems-Level Metabolic Analysis in Endocrine Disorders and Cancer

Lakhani,

Kang,

Kang

et al. 2023

Endocrinol Metab

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Metabolism is a dynamic network of biochemical reactions that support systemic homeostasis amidst changing nutritional, environmental, and physical activity factors. The circulatory system facilitates metabolite exchange among organs, while the endocrine system finely tunes metabolism through hormone release. Endocrine disorders like obesity, diabetes, and Cushing’s syndrome disrupt this balance, contributing to systemic inflammation and global health burdens. They accompany metabolic changes on multiple levels from molecular interactions to individual organs to the whole body. Understanding how metabolic fluxes relate to endocrine disorders illuminates the underlying dysregulation. Cancer is increasingly considered a systemic disorder because it not only affects cells in localized tumors but also the whole body, especially in metastasis. In tumorigenesis, cancer-specific mutations and nutrient availability in the tumor microenvironment reprogram cellular metabolism to meet increased energy and biosynthesis needs. Cancer cachexia results in metabolic changes to other organs like muscle, adipose tissue, and liver. This review explores the interplay between the endocrine system and systems-level metabolism in health and disease. We highlight metabolic fluxes in conditions like obesity, diabetes, Cushing’s syndrome, and cancers. Recent advances in metabolomics, fluxomics, and systems biology promise new insights into dynamic metabolism, offering potential biomarkers, therapeutic targets, and personalized medicine.

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Metformin exerts an antitumoral effect on papillary thyroid cancer cells through altered cell energy metabolism and sensitized by BACH1 depletion

Cited by 11 publications

References 48 publications

Metformin induces tumor immunogenic cell death in ovarian cancer by activating AMPK pathway

Metformin induces tumor immunogenic cell death in ovarian cancer by activating AMPK pathway

Transcription factor BACH1 in cancer: roles, mechanisms, and prospects for targeted therapy

Toward Systems-Level Metabolic Analysis in Endocrine Disorders and Cancer

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