The gene inhibin subunit beta B (INHBB) encodes the inhibin βB subunit, which is involved in forming protein members of the transforming growth factor-β (TGF-β) superfamily. The TGF-β superfamily is extensively involved in cell proliferation, differentiation, adhesion, movement, metabolism, communication, and death. Activins and inhibins, which belong to the TGF-β superfamily, were first discovered in ovarian follicular fluid. They were initially described as regulators of pituitary follicle-stimulating hormone (FSH) secretion both in vivo and in vitro. Later studies found that INHBB is expressed not only in reproductive organs such as the ovary, uterus, and testis but also in numerous other organs, including the brain, spinal cord, liver, kidneys, and adrenal glands. This wide distribution implies its involvement in the normal physiological functions of various organs; however, the mechanisms underlying these functions have not yet been fully elucidated. Recent studies suggest that INHBB plays a significant, yet complex role in tumorigenesis. It appears to have dual effects, promoting tumor progression in some contexts while inhibiting it in others, although these roles are not yet fully understood. In this paper, we review the different expression patterns, functions, and mechanisms of INHBB in normal and tumor tissues to illustrate the research prospects of INHBB in tumor progression.
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http://dx.doi.org/10.1007/s13105-024-01041-y | DOI Listing |
Hereditas
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Obstetrics and Gynecology Medical Centre, The First Affiliated Hospital of Hunan University of Traditional Chinese Medicine, No.105, Shaoshan Middle Road, Yuhua District, Changsha, 410007, Hunan, China.
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J Transl Med
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Department of Urology, The First Affiliated Hospital, Zhejiang University School of Medicine, Qingchun Road 79, Hangzhou, Zhejiang, 310003, China.
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View Article and Find Full Text PDFBiomark Res
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Department of Hematology and Medical Oncology, Emory University, 201 Dowman Dr, Atlanta, GA, 30322, USA.
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Biol Direct
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School of Medicine, South China University of Technology, Guangzhou, 510006, China.
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Mol Cancer
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Department of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.
Metabolic reprogramming within the tumor microenvironment (TME) is a hallmark of cancer and a crucial determinant of tumor progression. Research indicates that various metabolic regulators form a metabolic network in the TME and interact with immune cells, coordinating the tumor immune response. Metabolic dysregulation creates an immunosuppressive TME, impairing the antitumor immune response.
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