Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019204 (hepatocellular carcinoma)
71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ser/Thr protein phosphatase 5 (PPP5C) has been reported to participate in tumor progression. However, its functional role in hepatocellular carcinoma (HCC) remains unknown yet. In this study, we firstly evaluated the expression levels of PPP5C in six HCC cell lines by real-time PCR and found that PPP5C was widely expressed in HCC cells. To explore the role of PPP5C in HCC cell growth, lentivirus-mediated short hairpin RNA (shRNA) was employed to silence PPP5C expression in HepG2 and Bel-7404 cells. The expression of PPP5C was significantly downregulated in PPP5C knockdown cells. Knockdown of PPP5C markedly suppressed the proliferation and colony formation ability of HCC cells. Moreover, cell cycle analysis showed that PPP5C depletion in HepG2 cells led to G0/G1 phase and G2/M phase arrest. We demonstrate for the first time that PPP5C is essential for growth of HCC cells, which suggests that inhibition of PPP5C by RNAi may be a potential therapeutic strategy for the treatment of HCC.
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PMID:Knockdown of PPP5C inhibits growth of hepatocellular carcinoma cells in vitro. 2532 85

Serine/threonine protein phosphatase 5 (PPP5C) participates in multiple signaling pathways including cell cycle control and cell growth. PPP5C is involved in the progression of human breast cancer and hepatocellular carcinoma. However, its function in acute myelogenous leukemia (AML) remains unknown. In this study, we constructed a lentivirus system to knock down the expression level of PPP5C in leukemic cell line U937. Cell proliferation and cell cycles were assessed by MTT assay and flow cytometry respectively. Western blot was used to determine the level of caspase-3, PARP (poly ADP-ribose polymerase), CDK4 and CyclinD1. Knockdown of PPP5C suppressed the proliferation ability of U937 cells, and led to G0/G1 phase arrest, inducing cell apoptosis in U937 cells. The apoptosis of the U937 cells was associated with upregulating cleaved caspase-3 and PARP, and downregulating CDK4 and CyclinD1. In conclusions, PPP5C knockdown inhibits U937 cell proliferation and might be used as a potential therapeutic target for the treatment of leukemia.
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PMID:Knockdown of protein phosphatase 5 (PPP5C) suppresses the growth of leukemic cell line U937. 2775 48