LINC00339 regulates ROCK1 by miR‐152 to promote cell proliferation and migration in hepatocellular carcinoma

Background/Aims Emerging evidence have demonstrated that long noncoding RNAs are involved in the development and metastasis of various cancers including hepatocellular carcinoma (HCC). However, the role of LINC00339 in HCC progression is still unknown. Methods The LINC00339 expression in HCC cancer cells (HUH7, HepG2, HUH‐6, and SK‐Hep‐1) and tissues was assessed by quantitative real‐time polymerase chain reaction (qRT‐PCR). Functional experiments including cell counting Kit‐8 wound‐healing assay and transwell assay were used to explore the cell proliferation, migration, and invasion, respectively. The related molecular mechanisms were determined by Western blot. The RNA pull‐down assay, luciferase reporters assay, qRT‐PCR, and Western blot were performed to explore and confirm the interaction between LINC00339 and miR‐152, between miR‐152 and ROCK1. The role of LINC00339 in tumor formation and metastasis were explored through in vivo experiments. Results LINC00339 was highly expressed in HCC tissues and cell lines. LINC00339 promoted the cell proliferation, migration, and invasion of HCC cells, while knockout of LINC00339 showed the opposite trends. The proliferation and migration of HCC cells induced by LINC00339 overexpression were mostly reversed after transfected with miR‐152 mimics. LINC00339 exerted oncogenesis effect on HCC progression by targeting miR‐152/ROCK1, and the expression of LINC00339 was negatively correlated with miR‐152 expression and positively correlated with ROCK1 expression in clinical HCC samples. Moreover, we also proved that LINC00339 overexpression exacerbated the tumor formation and metastases in nude mice and LINC00339 silence showed the opposite results. Conclusion LINC00339 might act as a potential therapeutic target for HCC.