Advances in the functions of CTRP6 in the development and progression of the malignancy

Abstract

CTRP6, a member of the C1q/TNF-related protein (CTRP) family, has gained increasing scientific interest because of its regulatory role in tumor progression. Previous studies have shown that CTRP6 is closely involved in regulating various pathophysiological processes, including glucose and lipid metabolism, cell proliferation, apoptosis, and inflammation. To date, CTRP6 has been identified as related to eight different malignancies, including lung cancer, oral cancer, gastric cancer, colon cancer, liver cancer, bladder cancer, renal cancer, and ovarian cancer. CTRP6 is reported to be associated with tumor progression by activating a series of related signal networks. This review article mainly discusses the biochemistry and pleiotropic pathophysiological functions of CTRP6 as a new molecular mediator in carcinogenesis, hoping that the information summarized herein could make a modest contribution to the development of novel cancer treatments in the future.

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

“…CTRP6's role in tumorigenesis is multifaceted, with evidence suggesting that it can both promote and inhibit tumor growth, depending on the cancer type[ 9 ]. In the context of digestive system tumors, such as gastric and liver cancers, CTRP6 has been shown to be overexpressed and is implicated in tumor cell proliferation, migration, and angiogenesis[ 10 ]. The mechanistic link between CTRP6 and the PI3K pathway involves several key processes.…”

“…CTRP6's role in colorectal cancer is further amplified by its ability to regulate glycolipid metabolism, a process that is often deregulated in cancer cells[ 19 ]. The PI3K/Akt pathway is known to influence glucose and lipid metabolism, providing the necessary energy and building blocks for tumor cells[ 10 ]. CTRP6's modulation of these metabolic pathways can indirectly enhance the activity of the PI3K pathway, further fueling colorectal cancer development[ 20 ].…”