Hepatocellular carcinoma (HCC) is the most common
neoplasm and is a leading cause of
cancer-related death. Despite advances in the diagnosis and management of HCC, its prognosis remain unfavorable. Accumulating evidence has shown that long intergenic noncoding RNAs (
lincRNAs) play central roles in the development of HCC. In this study, we identified a long intergenic
noncoding RNA referred to as
lincRNA P7 in HCC and explored its clinical significance and biological functions in HCC. The expression level of
lincRNA P7 was significantly aberrantly deceased in HCC
cancer tissues and cells lines. Gain- and loss-of-function experiments revealed that overexpression of
lincRNA P7 significantly inhibited the proliferation of HCC-derived
cancer cells, whereas
lincRNA P7 knockdown promoted cell growth. Mechanistically,
lincRNA P7 blocked Erk1/2 signaling and repressed activation of the STAT1 pathway. In nude mouse models, we show that overexpression of
lincRNA P7 effectively repressed HCC xenograft
tumor growth in vivo. Moreover, a clinical investigation demonstrated that down-regulated
lincRNA P7 expression correlated with
liver cirrhosis, Hepatitis B virus (HBV)
infection, clinical stage of the
tumor and recurrence. A Kaplan-Meier survival analysis showed that the expression of
lincRNA P7 was significantly related to overall survival (P = 0.003) and recurrence-free survival (P = 0.031). Collectively, our findings suggested that the down-regulation of
lincRNA P7 predicts poor clinical outcomes for HCC patients and might be a powerful candidate prognostic
biomarker and target in HCC.