Background
Previous research has elaborated on the role of long non-coding RNA LINC00173 in the pathogenesis of various cancers; however, our knowledge of its clinical consequences and mechanisms in endometrial cancer (EC) is limited. Our current work is aimed at investigating the effect of LINC00173 in combination with its upstream gene HNRNPC on EC progression.
Conclusion
LINC00173 can impair the malignancy of EC cell by interacting with HNRNPC. This finding may contribute to the understanding of the tumorigenic effects of HNRNPC and LINC00173 on EC.
Methods
LINC00173 and HNRNPC levels were investigated by qRT-PCR or western blotting in EC tissues. The functional roles of HNRNPC and LINC00173 were assessed using transwell, colony formation and CCK-8 assays. A xenograft was used to verify the phenotype of LINC00173 after its overexpression. The regulatory role between HNRNPC and LINC00173 was investigated using RIP and RNA pull-down analysis.
Results
In EC tissues, LINC00173 expression was down-regulated. We observed that increased LINC00173 inhibited EC cell growth and migration. LINC00173 was a downstream target of HNRNPC, and its expression level was elevated by HNRNPC silencing. LINC00173 overexpression shifted part of HNRNPC into the cytoplasm from the nucleus of EC cells. Furthermore, HNRNPC expression was upregulated in EC and its silencing inhibited EC cell malignancy in vitro.