Long non-coding RNA HCP5 functions as a sponge of miR-29b-3p and promotes cell growth and metastasis in hepatocellular carcinoma through upregulating DNMT3A

Background: Multiple researches have revealed that long non-coding RNA (lncRNAs) served as regulatory factor in modulating tumorigenesis of hepatocellular carcinoma (HCC). In this study, we demonstrated that lncRNA HCP5 was a tumor promoting factor of HCC, and the molecular mechanism of HCP5 has been elucidated at length.Methods: BrdU, transwell assay and flow cytometry were exerted to estimate cell growth, metastasis, invasion and apoptosis of HCC in vitro. Animal studies were performed the effect of HCP5 in vivo. Furthermore, we identified that miR-29b-3p interacted with HCP5 or DNA methyltransferase 3A (DNMT3A) using dual luciferase assay. qRT-PCR, western blot, BrdU, tanswell and flow cytometry assays were used to investigate the correlation of HCP5/miR-29b-3p/DNMT3A axis. Results: In present research, we elaborated that HCP5 was overexpressed in HCC tissues and cell lines, and this phenomenon was even obvious in metastatic and recurrent cases. Knockdown of HCP5 significantly alleviated cell growth, metastasis and invasion through preventing apoptosis and activating EMT progress. Moreover, miR-29b-3p has been identified as a negatively regulatory target gene of HCP5, which served as tumor suppressor of HCC to prevent cell proliferation, migration and invasion. Subsequently, DNMT3A was found as a downstream regulatory factor of miR-29b-3p, of which study found that a participated element of HCC progression by activating AKT phosphorylation.Conclusion: Generally, our study elucidated for the first time that HCP5 plays a crucial role in HCC via HCP5/ miR-29b-3p/DNMT3A/AKT axis and demonstrated a novel diagnostic and therapeutic strategy with potentiality.