Regulation of the Cell Cycle by ncRNAs Affects the Efficiency of CDK4/6 Inhibition

Author:

Hu Qingyi1,Huang Tao1

Affiliation:

1. Department of Breast and Thyroid Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China

Abstract

Cyclin-dependent kinases (CDKs) regulate cell division at multiple levels. Aberrant proliferation induced by abnormal cell cycle is a hallmark of cancer. Over the past few decades, several drugs that inhibit CDK activity have been created to stop the development of cancer cells. The third generation of selective CDK4/6 inhibition has proceeded into clinical trials for a range of cancers and is quickly becoming the backbone of contemporary cancer therapy. Non-coding RNAs, or ncRNAs, do not encode proteins. Many studies have demonstrated the involvement of ncRNAs in the regulation of the cell cycle and their abnormal expression in cancer. By interacting with important cell cycle regulators, preclinical studies have demonstrated that ncRNAs may decrease or increase the treatment outcome of CDK4/6 inhibition. As a result, cell cycle-associated ncRNAs may act as predictors of CDK4/6 inhibition efficacy and perhaps present novel candidates for tumor therapy and diagnosis.

Publisher

MDPI AG

Subject

Inorganic Chemistry,Organic Chemistry,Physical and Theoretical Chemistry,Computer Science Applications,Spectroscopy,Molecular Biology,General Medicine,Catalysis

Reference316 articles.

1. Coordinating gene expression during the cell cycle;Fischer;Trends Biochem. Sci.,2022

2. Negative regulator of E2F transcription factors links cell cycle checkpoint and DNA damage repair;Wang;Proc. Natl. Acad. Sci. USA,2018

3. Signalling pathways linking integrins with cell cycle progression;Streuli;Matrix Biol.,2014

4. Targeting CDK4 and CDK6: From Discovery to Therapy;Sherr;Cancer Discov.,2016

5. Genomic Aberrations that Activate D-type Cyclins Are Associated with Enhanced Sensitivity to the CDK4 and CDK6 Inhibitor Abemaciclib;Gong;Cancer Cell,2017

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