The Effect of Long Non-Coding RNA (lncRNA) HCP5 on Regulating Epithelial-Mesenchymal Transition (EMT)-Related Markers in Gastric Carcinoma Is Partially Reversed by miR-27b-3p.

BACKGROUND lncRNA HCP5 plays a cancer-promoting role in a variety of cancers. This study was the first to explore the mechanism of HCP5 in gastric carcinoma (GC). MATERIAL AND METHODS The differences in HCP5 between GC patients and healthy people were revealed in the TCGA database. The expression of HCP5 in GC tissues and adjacent tissues was compared by qRT-PCR. At the same time, the clinic pathological features of the patients were counted. Starbase and luciferase assay predicted and verified that miR-27b-3p is a targeted miRNA for HCP5. The expression of HCP5 and miR-27b-3p in various GC cells was detected by qRT-PCR. Cell viability and metastasis in different treatment groups were assessed by use of Cell Couting Kit-8 assay and clone formation assay, wound-healing assay, and transwell assay. Finally, expression of epithelial-mesenchymal transition (EMT)-associated markers was detected by Western blot. RESULTS We found that HCP5 was overexpressed in GC tissues. Patients with higher expression of HCP5 had larger tumors, were more likely to have lymph node metastasis, and had higher TNM stage. HCP5 was overexpressed in GC cells, but this was reversed by miR-27b-3p. Silencing HCP5 inhibited GC cell viability and metastasis by downregulating Vimentin and N-cadherin and up-regulating E-cadherin, but this effect was partially reversed by miR-27b-3p inhibitor. CONCLUSIONS The effect of silencing HCP5 on repressing GC cells viability and metastasis by regulating EMT-associated markers can be partially reversed by miR-27b-3p inhibitor.