Inhibin subunit beta B (INHBB): an emerging role in tumor progression.
Ying LiuQing ZhouGuoying ZouWenling ZhangPublished in: Journal of physiology and biochemistry (2024)
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.
Keyphrases
- transforming growth factor
- poor prognosis
- epithelial mesenchymal transition
- spinal cord
- genome wide identification
- cell proliferation
- signaling pathway
- gene expression
- protein kinase
- case control
- transcription factor
- binding protein
- white matter
- multidrug resistant
- genome wide
- small molecule
- protein protein
- neuropathic pain
- pseudomonas aeruginosa
- staphylococcus aureus
- cerebral ischemia
- germ cell