C1QTNF6, also known as CTRP6, is a member of the CTRP family. It has been implicated in multiple biological processes including inflammation, glucose metabolism, endothelial cell modulation and carcinogenesis. It may be involved in pathways such as cytokine-cytokine receptor interaction, AKT/NF-κB signaling pathway [2,4].

Studies on C1QTNF6 in various cancers show its significance. In lung adenocarcinoma, knockdown of C1QTNF6 inhibits cell proliferation, migration and invasion, and overexpression promotes these cancer-related cellular behaviors. MiR-184 and miR-29a-3p can down-regulate C1QTNF6 expression, restraining cancer cell processes [1,2]. In oral squamous cell carcinoma, knockdown of C1QTNF6 decreases cell viability, causes cell cycle arrest at G2/M phase and enhances apoptosis, while in non-small cell lung cancer, inhibition of C1QTNF6 attenuates cell proliferation, migration, invasion and promotes apoptosis in vitro and in vivo [3,5]. In bladder cancer, high C1QTNF6 expression is associated with poor prognosis and knockdown reduces cell migration and invasion ability [6]. In clear cell renal cell carcinoma, C1QTNF6 is overexpressed, correlates with clinical progression and is an independent risk factor for overall survival [7]. In gastric carcinoma, C1QTNF6-knockdown decreases cell growth, proliferation and migration, and increases apoptosis [8]. In polycystic ovary syndrome (PCOS), C1QTNF6 is involved in the pathogenesis by affecting the inflammatory response of granulosa cells via the AKT/NF-κB signaling pathway [4].

In conclusion, C1QTNF6 plays important roles in cancer development and progression, as well as in the pathogenesis of PCOS. Functional studies, especially those using knockdown models in cancer cells, have revealed its pro-tumorigenic effects in multiple cancer types, highlighting its potential as a therapeutic target for these diseases [1-10].

References:

1. Rao, Xiao, Lu, Yunping. 2022. C1QTNF6 Targeted by MiR-184 Regulates the Proliferation, Migration, and Invasion of Lung Adenocarcinoma Cells. In Molecular biotechnology, 64, 1279-1287. doi:10.1007/s12033-022-00495-z. https://pubmed.ncbi.nlm.nih.gov/35578071/

2. Lin, Guofu, Lin, Lanlan, Lin, Hai, Zeng, Yiming, Xu, Yuan. 2022. C1QTNF6 regulated by miR-29a-3p promotes proliferation and migration in stage I lung adenocarcinoma. In BMC pulmonary medicine, 22, 285. doi:10.1186/s12890-022-02055-2. https://pubmed.ncbi.nlm.nih.gov/35879698/

3. Song, Xiaobin, Li, Longjie, Shi, Liang, Wei, Fengcai, Wang, Ketao. 2021. C1QTNF6 promotes oral squamous cell carcinoma by enhancing proliferation and inhibiting apoptosis. In Cancer cell international, 21, 666. doi:10.1186/s12935-021-02377-x. https://pubmed.ncbi.nlm.nih.gov/34906149/

4. Yan, Sisi, Ding, Jinli, Zhang, Yi, Yin, Tailang, Yang, Jing. . C1QTNF6 participates in the pathogenesis of PCOS by affecting the inflammatory response of granulosa cells‡. In Biology of reproduction, 105, 427-438. doi:10.1093/biolre/ioab094. https://pubmed.ncbi.nlm.nih.gov/33959757/

5. Zhang, Wei, Feng, Ganzhu. . C1QTNF6 regulates cell proliferation and apoptosis of NSCLC in vitro and in vivo. In Bioscience reports, 41, . doi:10.1042/BSR20201541. https://pubmed.ncbi.nlm.nih.gov/33269376/

6. Zhu, Xin, Tong, Hang, Gao, Shun, He, Weiyang, Gou, Xin. 2020. C1QTNF6 Overexpression Acts as a Predictor of Poor Prognosis in Bladder Cancer Patients. In BioMed research international, 2020, 7139721. doi:10.1155/2020/7139721. https://pubmed.ncbi.nlm.nih.gov/33123583/

7. Lin, Wanzun, Chen, Xiaochuan, Chen, Ting, Wu, Junxin, Qiu, Sufang. 2020. C1QTNF6 as a Novel Diagnostic and Prognostic Biomarker for Clear Cell Renal Cell Carcinoma. In DNA and cell biology, 39, 1000-1011. doi:10.1089/dna.2019.5299. https://pubmed.ncbi.nlm.nih.gov/32282241/

8. Qu, Hai-Xia, Cui, Lin, Meng, Xin-Ying, Wang, Dong, Jiang, Xiang-Jun. 2018. C1QTNF6 is overexpressed in gastric carcinoma and contributes to the proliferation and migration of gastric carcinoma cells. In International journal of molecular medicine, 43, 621-629. doi:10.3892/ijmm.2018.3978. https://pubmed.ncbi.nlm.nih.gov/30431096/