Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

Therapeutic Strategies for RB1-Deficient Cancers: Intersecting Gene Regulation and Targeted Therapy

Version 1 : Received: 16 March 2024 / Approved: 18 March 2024 / Online: 18 March 2024 (10:29:38 CET)

A peer-reviewed article of this Preprint also exists.

Huang, M.-F.; Wang, Y.-X.; Chou, Y.-T.; Lee, D.-F. Therapeutic Strategies for RB1-Deficient Cancers: Intersecting Gene Regulation and Targeted Therapy. Cancers 2024, 16, 1558. Huang, M.-F.; Wang, Y.-X.; Chou, Y.-T.; Lee, D.-F. Therapeutic Strategies for RB1-Deficient Cancers: Intersecting Gene Regulation and Targeted Therapy. Cancers 2024, 16, 1558.

Abstract

The retinoblastoma (RB) transcriptional corepressor 1 (RB1) is a critical tumor suppressor gene, governing diverse cellular processes implicated in cancer biology. Dysregulation or deletion in RB1 contributes to the development and progression of various cancers, making it a prime target for therapeutic intervention. RB1's canonical function in cell cycle control and DNA repair mechanisms underscores its significance in restraining aberrant cell growth and maintaining genomic stability. Understanding the complex interplay between RB1 and cellular pathways is beneficial to fully elucidate its tumor-suppressive role across different cancer types and for therapeutic development. As a result, investigating vulnerabilities arising from RB1 deletion-associated mechanisms offers promising avenues for targeted therapy. Recently, several findings highlighted multiple methods as a promising strategy for combating tumor growth driven by RB1 loss, offering potential clinical benefits in various cancer types. This review summarizes the multifaceted role of RB1 in cancer biology and its implications for targeted therapy.

Keywords

retinoblastoma; RB1; E2F; Targeted Therapy; Therapeutic Vulnerabilities; Spliceosome; Cell Cycle; Epigenetic Regulators; Ubiquitin-Proteasome Pathway

Subject

Biology and Life Sciences, Biology and Biotechnology

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