Conclusion
HCP5 is a cancer-suppressive lncRNA in SKCM. HCP5 overexpression decreased SKCM cell malignancy in vitro by upregulating RARRES3, possibly via sponging miR-1286.
Methods
Survival analysis was performed using The Cancer Genome Atlas (TCGA)-SKCM data and SKCM patients' clinical data. Primary SKCM cells were derived from patients' pathologic tissue specimens. HCP5 overexpression was achieved by lentiviral transduction. Malignancy of SKCM cells was evaluated in vitro by cell proliferation, colony formation, apoptosis and transwell invasion assays. RARRES3 knockdown was achieved by siRNA transfection. DIANA microT-CDS algorithm was used to predict miRNAs that might interact with HCP5 and 3' untranslated region of RARRES3 mRNA. microRNA target luciferase reporter assay and AGO2-RNA immunoprecipitation were used to verify the interaction between HCP5, 3' UTR of RARRES3 mRNA and miR-1286.
Objective
This research aimed to investigate the role and mechanism of long noncoding RNA (lncRNA) HCP5 in skin cutaneous melanoma (SKCM). Materials and
Results
HCP5 level was decreased in SKCM tissue specimens compared to noncancerous counterparts. Low expression of HCP5 was associated with SKCM patients' poor overall survival and disease progression. HCP5 overexpression significantly reduced the malignancy of primary SKCM cells in vitro. RARRES3 was found as a HCP5-co-expressing gene in SKCM cells. HCP5 overexpression significantly increased RARRES3 expression in SKCM cells. RARRES3 knockdown partially abolished the anti-SKCM effect of HCP5 overexpression. MiR-1286 was found interacting with both HCP5 and 3' UTR of RARRES3 mRNA.