Fam110b-KO Mouse

Fam110b, a member of the FAM110 family, is a component of centrosome-associated proteins. It localizes to centrosomes and spindle poles, and may be involved in cell cycle progression [4]. Ectopic expression of Fam110b has been shown to impair cell cycle progression in the G1 phase [4].

In cancer research, overexpression of Fam110b inhibits the proliferation and invasion of non-small cell lung cancer (NSCLC) cells by inactivating the Wnt/β-catenin signaling pathway, suggesting its antitumor function in NSCLC [1]. In castration-resistant prostate cancer, it appears to have an oncogenic role, regulating androgen receptor (AR) signaling and being regulated by androgens. Its siRNA inhibits the growth of prostate cancer cells, especially in androgen-deficient conditions [3]. Pan-cancer analysis shows that its transcription and protein expression vary among cancer types, having prognostic predictive value for some tumors like brain lower grade glioma, stomach adenocarcinoma, and pancreatic adenocarcinoma. In the tumor microenvironment, its expression is associated with immune cell infiltration, immune checkpoints, etc. [2]. In pancreatic adenocarcinoma, its expression trend decreases with tumor differentiation grades, and it is associated with patient survival time and has a diagnosis value [6]. In endometrial cancer, it is one of the genes in a prognostic risk scoring system related to patient prognosis and immune status, and may help identify patients who can benefit from immunotherapy [5].

In summary, Fam110b plays diverse roles in cell cycle and cancer biology. Functional studies, especially those using RNA interference as a form of loss-of-function experiment in cancer cells, have revealed its significance in tumor progression and the tumor microenvironment across multiple cancer types, highlighting its potential as a therapeutic target.

References:

1. Xie, Menghua, Cai, Lin, Li, Jingduo, Li, Ailin, Miao, Yuan. 2020. FAM110B Inhibits Non-Small Cell Lung Cancer Cell Proliferation and Invasion Through Inactivating Wnt/β-Catenin Signaling. In OncoTargets and therapy, 13, 4373-4384. doi:10.2147/OTT.S247491. https://pubmed.ncbi.nlm.nih.gov/32547070/

2. Li, Yuwei, Li, Xiaoxi, Wu, Bihua, Su, Yunpeng, Guo, Le. 2024. Pan-cancer analysis and single-cell analysis reveals FAM110B as a potential target for survival and immunotherapy. In Frontiers in molecular biosciences, 11, 1424104. doi:10.3389/fmolb.2024.1424104. https://pubmed.ncbi.nlm.nih.gov/39170745/

3. Vainio, Paula, Wolf, Maija, Edgren, Henrik, Iljin, Kristiina, Kallioniemi, Olli. 2011. Integrative genomic, transcriptomic, and RNAi analysis indicates a potential oncogenic role for FAM110B in castration-resistant prostate cancer. In The Prostate, 72, 789-802. doi:10.1002/pros.21487. https://pubmed.ncbi.nlm.nih.gov/21919029/

4. Hauge, Helena, Patzke, Sebastian, Aasheim, Hans-Christian. 2007. Characterization of the FAM110 gene family. In Genomics, 90, 14-27. doi:. https://pubmed.ncbi.nlm.nih.gov/17499476/

5. Chi, Hao, Gao, Xinrui, Xia, Zhijia, Yang, Guanhu, Wang, Qin. 2023. FAM family gene prediction model reveals heterogeneity, stemness and immune microenvironment of UCEC. In Frontiers in molecular biosciences, 10, 1200335. doi:10.3389/fmolb.2023.1200335. https://pubmed.ncbi.nlm.nih.gov/37275958/

6. Xi, Ting, Zhang, Guizhi. 2018. Integrated analysis of tumor differentiation genes in pancreatic adenocarcinoma. In PloS one, 13, e0193427. doi:10.1371/journal.pone.0193427. https://pubmed.ncbi.nlm.nih.gov/29596435/