Purpose: The aim was to research the role of LINC01116 in the prognosis of colorectal cancer (CRC) patients and development of colorectal cancer cells.
Methods: In total 62 colorectal cancer patient tissues and human CRC cell lines (OUMS23, SW116, SW480 and LOVO) were obtained for this study. SiLINC01116, miR-9-5p mimic, LINC01116, oe-STMN1 and their controls were transfected. The qRT-PCR method and Western blot were used to detect the levels of LINC01116, miR-9-5p and STMN1 in tissues and cells. CCK8 assay and flow cytometry were processed for proliferation and apoptosis, respectively. Transwell assay was undertaken to verify invasion and migration. Luciferase assay and pull down assay were processed to confirm the binding relationship among LINC01116, miR-9-5p and . Immunohistochemistry assay also detected the expression of . Kaplan-Meier survival curve was used to analyze patient survival rate. Pearson correlation analysis was used to evaluate the regulatory relationship between LINC01116, miR-9-5p and in tissues.
Results: LINC01116 was expressed higher in CRC tissues and cells. Patients with higher expression of LINC01116 had worse prognosis. Knockdown of LINC01116 suppressed development of CRC cell. LINC01116 negatively regulated miR-9-5p, while MiR-9-5p was negatively related to . miR-9-5p mimic could rescue the effect of LINC01116, inhibit migration and invasion, and improve apoptosis of CRC cells. Oe-STMN1 could also rescue the effect of miR-9-5p on the development of colorectal cancer.
Conclusion: LINC01116 promoted the development of colorectal cancer via modulating miR-9-5p/ axis.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7573327 | PMC |
| http://dx.doi.org/10.2147/OTT.S253532 | DOI Listing |
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