Abstract
The cAMP-regulated phosphoprotein 19 (ARPP-19) plays a key role in cell mitotic G2/M transition. Expression of ARPP-19 was increased in human hepatocellular carcinoma (HCC) compared to adjacent non-tumorous liver tissues in 36 paired liver samples, and the level of ARPP-19 in HCC tissues was positively correlated with the tumor size. To determine the interrelationship between ARPP-19 expression and HCC, we silenced ARPP-19 expression in the human hepatocarcinoma HepG2 and SMMC-7721 cells using lentivirus encoding ARPP-19 siRNA. HepG2 and SMMC-7721 cells with ARPP-19 knockdown displayed lowered cell growth rate, retarded colony formation and increased arrest at the G2/M phase transition. Silencing ARPP-19 in HCC cells resulted in decreased protein levels of phospho-(Ser) CDKs substrates and increased levels of inactivated cyclin division cycle 2 (Cdc2). Therefore, ARPP-19 may play a role in HCC pathogenesis through regulating cell proliferation.
Highlights
Hepatocellular carcinoma (HCC) remains the sixth most common malignancy and third most frequent cause of cancer-related death worldwide [1]
The expression of ARPP-19 was compared between 36 pairs of hepatocellular carcinoma (HCC) and the corresponding non-tumorous liver tissue (NT) of the same patient
The results of Quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR) (Figure 2A) demonstrated that the ARPP-19 mRNA level was significantly increased in HCC, as compared to that in the relative normal liver tissue (p < 0.01)
Summary
Hepatocellular carcinoma (HCC) remains the sixth most common malignancy and third most frequent cause of cancer-related death worldwide [1]. Surgical resection or local ablation therapy is effective only at early stages, and approximately 70% of these patients develop recurrent tumors within five years [2,3]. No effective treatment is available for HCC patients at advanced stage, and molecular target therapy has been considered as a potential intervention for HCC patients. Cellular or molecular mechanisms underlying HCC development are still poorly defined, and therapeutic strategies for prevention or treatment of advanced-stage HCC are largely lacking [4]. The only proven effective target medicine for HCC, Sorafenib, could prolong the median overall survival for merely
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