Cks1b-KO Mouse

Cks1b, Cyclin-dependent kinase regulatory subunit 1B, is a member of the conserved cyclin kinase subunit 1 (CKS1) protein family. It plays an essential role in cell cycling and is associated with multiple signaling pathways relevant to cell growth, apoptosis, and metastasis. Given its role in cell cycle regulation, genetic models such as gene knockout (KO) or conditional knockout (CKO) mouse models could potentially be valuable for further exploring its function [1].

Numerous studies show Cks1b's significant association with cancer. Knockdown of Cks1b in hepatocellular carcinoma cell lines inhibited cell survival, proliferation, migration, invasion, and induced apoptosis, suggesting it acts as an oncogene by activating the JAK/STAT3 signal pathway [2]. In pancreatic cancer, Cks1b knockdown reduced cell viability and invasion via regulating PD-L1 expression, and its high expression was related to histologic grading, prognosis, and TMB [3]. Also, in retinoblastoma cells, downregulation of Cks1b restrained proliferation, migration, invasion, and angiogenesis through the MEK/ERK signaling pathway [6].

In conclusion, Cks1b is crucial in cell cycling and is significantly involved in the pathogenesis of multiple cancers. Findings from functional studies, especially those using loss-of-function models, highlight its role in promoting cancer cell proliferation, migration, and invasion, and in conferring drug resistance. This knowledge provides potential therapeutic targets for improving cancer treatment [1,2,3,4,5,6].

References:

1. Shi, Wenwen, Huang, Qiudi, Xie, Jiacui, Yu, Xiyong, Zhou, Yi. 2020. CKS1B as Drug Resistance-Inducing Gene-A Potential Target to Improve Cancer Therapy. In Frontiers in oncology, 10, 582451. doi:10.3389/fonc.2020.582451. https://pubmed.ncbi.nlm.nih.gov/33102238/

2. Liu, Xitao, Zhao, Defang. 2021. CKS1B promotes the progression of hepatocellular carcinoma by activating JAK/STAT3 signal pathway. In Animal cells and systems, 25, 227-234. doi:10.1080/19768354.2021.1953142. https://pubmed.ncbi.nlm.nih.gov/34408811/

3. Li, Lincheng, Wang, Jing, Zhang, Zhuochao, Li, Chonghui, Liu, Rong. 2022. Identification of CKS1B as a prognostic indicator and a predictive marker for immunotherapy in pancreatic cancer. In Frontiers in immunology, 13, 1052768. doi:10.3389/fimmu.2022.1052768. https://pubmed.ncbi.nlm.nih.gov/36405738/

4. Zhang, Liuxi, Wei, Fang, Sun, Qihui, Xie, Keping, He, Jie. 2025. FOXM1-Driven CKS1B Upregulation Promotes Pancreatic Cancer Progression and Therapeutic Resistance. In International journal of biological sciences, 21, 1047-1064. doi:10.7150/ijbs.105289. https://pubmed.ncbi.nlm.nih.gov/39897042/

5. Tang, Yuzhu, Lan, Xiaohua, Yan, Maohui, Fu, Zhiguang, Li, Hongqi. . CKS1B as a potential target for prognostic assessment and intervention in pancreatic cancer and its role in abnormal proliferation and cellular phenotype through mediation of cell cycle signaling pathways. In Saudi medical journal, 45, 128-138. doi:10.15537/smj.2024.45.2.20230132. https://pubmed.ncbi.nlm.nih.gov/38309745/

6. Zeng, Zhou, Gao, Zhao-Lin, Zhang, Zhi-Pei, Yang, Jie, Xia, Xiao-Bo. 2019. Downregulation of CKS1B restrains the proliferation, migration, invasion and angiogenesis of retinoblastoma cells through the MEK/ERK signaling pathway. In International journal of molecular medicine, 44, 103-114. doi:10.3892/ijmm.2019.4183. https://pubmed.ncbi.nlm.nih.gov/31115482/