Conclusion
lncRNA SLC16A1-AS1 contributes to the initiation and progression of CRC by modulating miR-515-5p to regulate MAP3K9 expression, providing potential insights for CRC treatment.
Methods
Cell viability was tested using Cell Counting Kit-8 (CCK-8). Cell invasion and migration were evaluated using Transwell assays, and apoptosis was determined by flow cytometry. Gene expression was tested by qRT-PCR or Western blot. The targeting relationship between miR-515-5p and MAP3K9 was verified using bioinformatics tools, RNA immunoprecipitation (RIP) experiments, and dual-luciferase reporter assays.
Objective
To investigate the role of long non-coding RNA (lncRNA) SLC16A1-AS1 in the initiation and progression of colorectal cancer (CRC).
Results
Both lncRNA SLC16A1-AS1 and MAP3K9 were upregulated in CRC cells, while miR-515-5p expression was downregulated. Overexpression of miR-515-5p and silencing of lncRNA SLC16A1-AS1 inhibited CRC cell proliferation, suppressed cell invasion and migration, and promoted cell apoptosis. The targeting relationship between lncRNA SLC16A1-AS1 and miR-515-5p, as well as between MAP3K9 and miR-515-5p, were confirmed by bioinformatics, RIP assays, and luciferase reporter assays.