BIN1 in cancer: biomarker and therapeutic target.

Autor: Chen SY; Department of Urology, The Second Hospital of Lanzhou University, Lanzhou, China., Cao JL; Department of Urology, The Second Hospital of Lanzhou University, Lanzhou, China., Li KP; Department of Urology, The Second Hospital of Lanzhou University, Lanzhou, China., Wan S; Department of Urology, The Second Hospital of Lanzhou University, Lanzhou, China., Yang L; Department of Urology, The Second Hospital of Lanzhou University, Lanzhou, China. ery_yangli@lzu.edu.cn.
Jazyk: angličtina
Zdroj: Journal of cancer research and clinical oncology [J Cancer Res Clin Oncol] 2023 Aug; Vol. 149 (10), pp. 7933-7944. Date of Electronic Publication: 2023 Mar 09.
DOI: 10.1007/s00432-023-04673-7
Abstrakt: Background: The bridging integrator 1 (BIN1) protein was originally identified as a pro-apoptotic tumor suppressor that binds to and inhibits oncogenic MYC transcription factors. BIN1 has complex physiological functions participating in endocytosis, membrane cycling, cytoskeletal regulation, DNA repair deficiency, cell-cycle arrest, and apoptosis. The expression of BIN1 is closely related to the development of various diseases such as cancer, Alzheimer's disease, myopathy, heart failure, and inflammation.
Purpose: Because BIN1 is commonly expressed in terminally differentiated normal tissues and is usually undetectable in refractory or metastatic cancer tissues, this differential expression has led us to focus on human cancers associated with BIN1. In this review, we discuss the potential pathological mechanisms of BIN1 during cancer development and its feasibility as a prognostic marker and therapeutic target for related diseases based on recent findings on its molecular, cellular, and physiological roles.
Conclusion: BIN1 is a tumor suppressor that regulates cancer development through a series of signals in tumor progression and microenvironment. It also makes BIN1 a feasible early diagnostic or prognostic marker for cancer.
(© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)
Databáze: MEDLINE
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