LINC00858 promotes colorectal cancer by sponging miR-4766-5p to regulate PAK2.

OBJECTIVES

LncRNAs (long noncoding RNAs) have been reported to critically regulate colorectal cancer (CRC). We prospectively investigated effects and mechanisms of lncRNA LINC00858 on regulation of CRC progression.

METHODS

Expression of LINC00858 and its target were analyzed by quantitative real-time polymerase chain reaction and in situ hybridization. MTT and bromodeoxyuridine/5-bromo-2'-deoxyuridine (BrdU) staining to assess cell proliferation ability. Flow cytometry, wound healing, and transwell assays were conducted to evaluate cell apoptosis, migration, and invasion, respectively. Interaction between LINC00858 and its target was confirmed by luciferase activity assay and RNA immunoprecipitation. Subcutaneous xenotransplanted tumor model was established and employed to detect tumorigenic functions of LINC00858, and further evaluated by qRT-PCR, western blot, immunohistochemistry, and hematoxylin and eosin staining.

RESULTS

With a predicted poor prognosis, LINC00858 was upregulated in CRC patients. LINC00858 knockdown suppressed cell proliferation, invasion, and migration abilities, meanwhile induced cell apoptosis. Moreover, LINC00858 could target and inhibit the miR-4766-5p expression, thus promoting CRC progression. miR-4766-5p further suppressed serine/threonine kinase PAK2. Interestingly, interference of LINC00858 suppressed tumorigenic ability of CRC in vivo by downregulating PAK2.

CONCLUSIONS

LINC00858 promoted CRC progression by sponging miR-4766 to upregulate PAK2, shedding lights on LINC00858 as a potential therapeutic target candidate in CRC treatment from bench to clinic.