LINC00958 Targets miR-145-3p/CDK1 Axis to Aggravate the Malignancy of Colon Cancer.

OBJECTIVE

Studies summarize that LINC00958 manifests considerable oncogenic potential in diverse cancers. However, its role in colon cancer (CC) is rarely studied. Herein, we attempted to disclose LINC00958's mechanism of action and function in the development of CC.

METHODS

The relative expressions of LINC00958, CDK1 mRNA, and miR-145-3p were quantified by means of RT-qPCR. CDK1 protein levels were determined via western blotting. CCK-8, wound healing, and transwell experiments were conducted to assess the abilities of cells to proliferate, migrate, and invade. To ascertain the role of LINC00958, xenograft assays were performed. The predicted binding relationships of miR-145-3p with LINC00958 and CDK1 were confirmed by means of dual-luciferase reporter and RIP studies.

RESULTS

A reinforced expression of LINC00958 was observed among CC cells and tumor samples. The deficiency in LINC00958 not only restrained the invasion, migration, and proliferation of the cancer cells but also impeded the development of tumors . LINC00958 directly bound to miR-145-3p, which was downregulated in CC. Consequently, the depletion in miR-145-3p attenuated the anti-cancer effects induced by the shortage of LINC00958. MiR-145-3p directly interacted with downstream functional molecule CDK1. CDK1 expression was enhanced in CC. It exerted oncogenic properties by stimulating CC cell proliferation, invasion, and survival. Meanwhile, miR-145-3p negatively modulated the expression of CDK1, thus attenuating the oncogenic effects produced by CDK1 in CC.

CONCLUSIONS

LINC00958 interacts with miR-145-3p and modulates the miR-145-3p/CDK1 axis. Hence, LINC00958 contributes to CC's malignant progression.