Conclusion
LncRNA SNHG4 sponges miR-144-3p and upregulates MET to promote the proliferation, colony formation, invasion, and immune escape of CRC cells, leading to the progression of CRC.
Methods
CRC tissues were collected and the expression levels of lncRNA SNHG4, miR-144-3p, and MET were detected by quantitative real-time PCR (qRT-PCR). Then, the localization of lncRNA SNHG4 was studied by fluorescence in situ hybridization (FISH), and the regulatory relationship among lncRNA SNHG4, miR-144-3p, and MET was verified by dual-luciferase reporter assay. Next, cell counting kit-8 (CCK-8), Clone formation assay, and Transwell migration assay were carried out to evaluate cell proliferation, colony formation, and invasion, respectively. Flow cytometry was performed to evaluate cell apoptosis. Western blotting was applied to semi-quantify the expression levels of MET and PD-L1 in cells.
Objective
This study aimed to explore the underlying mechanism of long noncoding RNA (lncRNA) SNHG4 regulating MET to participate in the malignant biologic behaviors and immune escape of colorectal cancer (CRC) by sponging miR-144-3p.
Results
LncRNA SNHG4 expression was upregulated in CRC tissues. Knockdown of lncRNA SNHG4 suppressed the proliferation, colony formation and invasion of CRC cells (all P<0.05). LncRNA SNHG4 directly regulated miR-144-3p, by which either lncRNA SNHG4 knockdown or miR-144-3p overexpression can inhibit CD4+ T cell apoptosis (both P<0.05) to suppress immune escape. Either overexpression of lncRNA SNHG4 or knockdown of miR-144-3p activated PD-1/PD-L1 and induced CD4+ T cell apoptosis (both P<0.05). LncRNA SNHG4 targeted and regulated MET through the regulation of miR-144-3p, while overexpression of MET can partially reverse the effect of lncRNA SNHG4 knockdown on CD4+ T cells.