Tumor-related factor complement Clq/TNF-related protein 6 affects the development of digestive system tumors through the phosphatidylinositol 3-kinase pathway

IF 4.3 3区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY
Mowei Kong, Xin-Rui Li, Yu Gao, Ting-Fang Yang
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引用次数: 0

Abstract

In this editorial, we review the work of Razali et al published in World J Gastroenterology , 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.
肿瘤相关因子补体 Clq/TNF 相关蛋白 6 通过磷脂酰肌醇 3- 激酶途径影响消化系统肿瘤的发展
在这篇社论中,我们回顾了 Razali 等人发表在《世界胃肠病学杂志》(World J Gastroenterology)上的研究成果,尤其关注磷脂酰肌醇 3- 激酶(PI3K)通路中的 rs10889677 变异和布帕利西对结肠炎相关癌症的影响。PI3K 参与调控癌细胞的存活、分化和增殖,在促进癌症进展方面的作用已得到广泛认可。补体Clq/TNF相关蛋白6(CTRP6)是一种较新的肿瘤相关因子。最近的研究发现,CTRP6 通过 PI3K 通路在胃癌、肝癌、结直肠癌和其他消化道肿瘤中具有促癌作用。本文通过总结最新研究,试图揭示 CTRP6 通过 PI3K 途径影响消化系统肿瘤发生发展的机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
World Journal of Gastroenterology
World Journal of Gastroenterology 医学-胃肠肝病学
CiteScore
7.80
自引率
4.70%
发文量
464
审稿时长
2.4 months
期刊介绍: The primary aims of the WJG are to improve diagnostic, therapeutic and preventive modalities and the skills of clinicians and to guide clinical practice in gastroenterology and hepatology.
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