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Research progress on the regulatory mechanisms of FOXC1 expression in cancers and its role in drug resistance.

Authors :
Yang, Yihui
Li, Wan
Yang, Hong
Zhang, Yizhi
Zhang, Sen
Xu, Fang
Hao, Yue
Cao, Wanxin
Du, Guanhua
Wang, Jinhua
Source :
Gene. Mar2024, Vol. 897, pN.PAG-N.PAG. 1p.
Publication Year :
2024

Abstract

• The Forkhead box C1 (FOXC1) transcription factor is an important member of the FOX family and is involved in the development of more than 16 types of cancers. • The expression of FOXC1 expression in cancer is regulated at multiple levels including transcriptional regulation, post-transcriptional regulation and post-translational modification. • Dysregulation of FOXC1 is implicated in drug resistance in various types of cancer, especially in breast cancer. The Forkhead box C1 (FOXC1) transcription factor is an important member of the FOX family. After initially being identified in triple-negative breast cancer (TNBC) with significant oncogenic function, FOXC1 was subsequently demonstrated to be involved in the development of more than 16 types of cancers. In recent years, increasing studies have focused on the deregulatory mechanisms of FOXC1 expression and revealed that FOXC1 expression was regulated at multiple levels including transcriptional regulation, post-transcription regulation and post-translational modification. Moreover, dysregulation of FOXC1 is also implicated in drug resistance in various types of cancer, especially in breast cancer, which further emphasizes the translational and clinical significance of FOXC1 as a therapeutic target in cancer treatment. This review summarizes recent findings on mechanisms of FOXC1 dysregulation in cancers and its role in chemoresistance, which will help to better understand the oncogenic role of FOXC1, overcome FOXC1-mediated drug resistance and develop targeted therapy for FOXC1 in cancers. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
03781119
Volume :
897
Database :
Academic Search Index
Journal :
Gene
Publication Type :
Academic Journal
Accession number :
174793289
Full Text :
https://doi.org/10.1016/j.gene.2023.148079