Kong Mo-Wei, Li Xin-Rui, Gao Yu, Yang Ting-Fang
Department of Cardiology, Guiqian International General Hospital, Guiyang 550018, Guizhou Province, China.
Department of Endocrinology, The Affiliated Hospital of Chengde Medical College, Chengde 067000, Hebei Province, China.
World J Gastroenterol. 2024 Jul 14;30(26):3206-3209. doi: 10.3748/wjg.v30.i26.3206.
In this editorial, we review the work of Razali published in , with a particular focus on the effect of rs10889677 variation in the phosphatidylinositol 3-kinase (PI3K) pathway and buparlisib on colitis-associated cancer. The role of PI3K in promoting cancer progression has been widely recognized, as it is involved in regulating the survival, differentiation, and proliferation of cancer cells. The complement Clq/TNF-related protein 6 (CTRP6) is a newer tumor-associated factor. Recent studies have revealed the pro-tumor effect of CTRP6 in gastric cancer, hepatocellular carcinoma, colorectal cancer, and other gastrointestinal tumors through the PI3K pathway. This article attempts to reveal the mechanism through which the CTRP6 affects the development of digestive system tumors through the PI3K pathway by summarizing recent research.
在这篇社论中,我们回顾了拉扎利发表的研究工作,特别关注磷脂酰肌醇3激酶(PI3K)途径中的rs10889677变异以及布帕利昔对结肠炎相关癌症的影响。PI3K在促进癌症进展中的作用已得到广泛认可,因为它参与调节癌细胞的存活、分化和增殖。补体Clq/TNF相关蛋白6(CTRP6)是一种较新的肿瘤相关因子。最近的研究揭示了CTRP6通过PI3K途径在胃癌、肝细胞癌、结直肠癌和其他胃肠道肿瘤中的促肿瘤作用。本文试图通过总结近期研究来揭示CTRP6通过PI3K途径影响消化系统肿瘤发生发展的机制。