Long non-coding RNA LINC00858 promotes cells proliferation and invasion through the miR-153-3p/Rabl3 axis in hepatocellular carcinoma.

OBJECTIVE

Long non-coding RNA (lncRNA) LINC00858 is a cancer-associated lncRNA frequently dysregulated in many types of human cancers. In the current study, we aimed to explore the role of LINC00858 in hepatocellular carcinoma (HCC).

PATIENTS AND METHODS

The relative expression levels of LINC00858 in HCC samples and adjacent non-tumor samples were determined by qRT-PCR. Loss-of-function assay was performed to examine the function of LINC00858 in HCC in vitro. Bioinformatic analysis and the following Luciferase activity reporter assay were utilized to explore the downstream molecules of LINC00858. CCK-8 assay was performed to detect cell proliferation of HCC cells. Transwell assay was performed to evaluate the invasive ability of HCC cells.

RESULTS

Our results showed that LINC00858 was highly expressed in both HCC tissues and cell lines. Knockdown of LINC00858 inhibited the proliferation and invasion of HCC cells. Moreover, LINC00858 was found to act as a sponge of miR-153-3p, which directly bound to Rabl3 and regulated the Rabl3 expression. Furthermore, inhibition of miR-153-3p counteracted the effects of LINC00858 knockdown on proliferation and invasion of HCC cells. In addition, the overexpression of Rabl3 rescued the effects of miR-153-3p on cell proliferation and invasion of HCC cells.

CONCLUSIONS

In summary, these findings showed that LINC00858 exerted an ontogenetic role in HCC via regulating miR-153-3p/Rabl3 axis. Thus, LINC00858 might be utilized as a therapeutic target for the treatment of HCC.