LINC00704 boosts the immunologic escape of colorectal cancer cells by upregulating TLR4 by binding with miR- 203a- 3p

Abstract

Abstract Background Colorectal cancer (CRC) is a common malignant tumor and is the second most common cause of cancer-related deaths worldwide. Immune escape suppresses anti-tumor immunity and facilitates tumor cells to proliferate. MiR- 203a- 3p regulates cancer progression and LINC00704 may bind with miR- 203a- 3p to inhibit its effects. Methods In this study, the levels of miR- 203a- 3p and LINC00704 were tested in tumor tissue and non-cancer tissues in vivo. In further in vitro experiments, transfection, cell vitality, apoptosis, and proliferation ability were detected. The expression level of TLR4 was also examined. Finally, a luciferase assay was conducted to detect whether LINC00704 could bind with miR- 203a- 3p. Results A rise in LINC00704 mRNA was observed in CRC tissues while miR- 203a- 3p was reduced. LINC00704 boosts the proliferation of cells and inhibits cell apoptosis. LINC00704 regulates Toll- 1ike receptor- 4 (TLR4) expression through miR- 203a- 3p, thereby modulating cell viability. CRC cell immune escape was facilitated by LINC00704 via miR- 203a- 3p. Conclusion LINC00704 promotes CRC cell immunologic escape by upgrading TLR4 by binding with miR- 203a- 3p.

Keywords

• LINC00704
• Immune escape
• Colorectal cancer
• TLR4
• MiR- 203a- 3p