ACSL3 regulates CRC Cell Proliferation through ACSL3-LPIAT1 Signaling Pathway

Abstract

Background: Colorectal cancer (CRC) is a common cancer in China, with a high mortality rate. Lipid metabolism disorders can promote cancer metabolism reprogramming, and lipid metabolism related genes are prognostic biomarkers of cancer.

Objective: To investigate whether ACSL3 is involved in EMT and metastasis of CRC, and to explore the molecular mechanism of ACSL3 involvement in CRC.

Method: Establish CRC models with high expression of ACSL3 and knockdown of ACSL3. CCK8, flow cytometry, scratch assay, and Transwell assay were used to measure the effect of ACSL3 on CRC cells. In vivo experimental analysis of changes in tumor volume and weight caused by overexpression or knockdown of ACSL3. In addition, we also studied whether ACSL3 affects the change of Prostaglandin through participating in ACSL3-LPAIAT1 signal axis, and then affects the occurrence and progression of tumors.

Result: The apoptosis rate of cell lines with high expression of ACSL3 is significantly reduced. Overexpression of ACSL3 significantly enhances the migration and invasion ability of CRC cells. Silencing ACSL3 can partially reverse the increased invasiveness caused by overexpression of ACSL3. Overexpression of ACSL3 can increase the expression levels of LPIAT1 and cPLA2, which can be partially reversed by silencing ACSL3. In vivo experiments have also found that upregulation of ACSL3 has the effect of accelerating tumor volume and weight.

Conclusion: ACSL3 plays an important role in the progression of CRC, and may be a prognostic biomarker, becoming a new potential therapeutic target for the treatment of CRC.