CKS1B as Drug Resistance-Inducing Gene-A Potential Target to Improve Cancer Therapy.

Wenwen Shi,Qiudi Huang,Yi Zhou,Jiacui Xie,He Wang,Xiyong Yu

doi:10.3389/fonc.2020.582451

Abstract

Cancer is a threat to human health and life. Although previously centered on chemical drug treatments, cancer treatment has entered an era of precision targeted therapy. Targeted therapy entails precise guidance, allowing the selective killing of cancer cells and thereby reducing damage to healthy tissues. Therefore, the need to explore potential targets for tumor treatment is vital. Cyclin-dependent kinase regulatory subunit 1B (CKS1B), a member of the conserved cyclin kinase subunit 1 (CKS1) protein family, plays an essential role in cell cycling. A large number of studies have shown that CKS1B is associated with the pathogenesis of many human cancers and closely related to drug resistance. Here, we describe the current understanding of the cellular functions of CKS1B and its underlying mechanisms, summarize a recent study of CKS1B as a target for cancer treatment and discuss the potential of CKS1B as a therapeutic target.

Highlights

In recent years, the incidence of cancer has increased annually
Use of Long Non-coding RNAs (Lncrnas) Targeting Cyclin-dependent kinase regulatory subunit 1B (CKS1B) for Cancer Treatment LncRNAs, which are present at lower cellular concentrations and exhibit higher tissue specificity than protein-encoding RNAs, participate in cell differentiation, proliferation, and apoptosis under different conditions
As is a member of the Cks/Suc1 family of proteins, CKS1B plays an important role in the regulation of cell cycle progression

Summary

Introduction

The incidence of cancer has increased annually. According to national cancer statistics released by the National Cancer Center in 2019, in 2015, 3.929 million new malignant tumors were diagnosed in individuals 0−47 years of age in China, corresponding to an incidence of 285.83/100,000. CDKs are a family of proteases related to the cell cycle that can degrade CDK substrates and proteins regulated by upstream CDKs. The Cdc kinase subunit (CKS) protein has been isolated and shown to inhibit fission and germination yeast cyclin-dependent kinase 1 (CDK1) gene mutations [7, 8]. Clinical studies have found that the current treatments for MM are ineffective in killing cells that express CKS1B, leading to poor patient prognosis [23, 31].

Results

Conclusion