Cks1b-KO Mouse

Cks1b, or 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. Abnormal Cks1b expression has been linked to various diseases, making it an important target for research [1].

Numerous studies across different cancers have demonstrated the oncogenic role of Cks1b. In hepatocellular carcinoma, knockdown of Cks1b inhibited cell survival, proliferation, migration, and invasion, and induced apoptosis, with the mechanism involving the JAK/STAT3 signal pathway [2]. In pancreatic cancer, Cks1b was highly expressed in tumor tissue, and its knockdown reduced cell viability and invasion, and was associated with autophagy, T cell receptor signaling, immune cell infiltration, and drug sensitivity [3]. In papillary thyroid carcinoma, Cks1b promoted cell viability and invasion through activation of STAT3/PD-L1 signaling and Akt phosphorylation [4]. In retinoblastoma, downregulation of Cks1b restrained cell proliferation, migration, invasion, and angiogenesis via the MEK/ERK signaling pathway [5]. Also, in cutaneous squamous cell carcinoma, Cks1b amplification was associated with aggressive behavior and metastatic spread [6].

In conclusion, Cks1b is crucial in regulating cell cycling and is significantly involved in the pathogenesis of multiple cancers, promoting cancer cell proliferation, invasion, and metastasis. These findings from functional studies, especially those using knockdown models, highlight Cks1b as a potential therapeutic target for improving cancer therapy.

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. Wang, Hui, Zhang, Zhengdong, Yan, Zhe, Ma, Shihong. 2020. CKS1B promotes cell proliferation and invasion by activating STAT3/PD-L1 and phosphorylation of Akt signaling in papillary thyroid carcinoma. In Journal of clinical laboratory analysis, 35, e23565. doi:10.1002/jcla.23565. https://pubmed.ncbi.nlm.nih.gov/32960462/

5. 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/

6. Salgado, Rocío, Toll, Agustí, Alameda, Francesc, Pujol, Ramon M, Espinet, Blanca. . CKS1B amplification is a frequent event in cutaneous squamous cell carcinoma with aggressive clinical behaviour. In Genes, chromosomes & cancer, 49, 1054-61. doi:10.1002/gcc.20814. https://pubmed.ncbi.nlm.nih.gov/20737481/