Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P42574 (caspase-3)
 45,978 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

The targeting protein of serine/threonine protein phosphatase 5 (PPP5C) has been reported to be present in various malignancies. However, its functional role in pancreatic cancer (PC) remains unknown. In the present study, the function of PPP5C in PC cells treated with the first-line drug gemcitabine (GEM) was investigated. Short hairpin (sh)RNA targeting PPP5C was constructed to knockdown PPP5C in PANC-1 cells. Cell cycle and apoptosis analyses were performed in order to investigate the mechanisms underlying the effects induced by PPP5C silencing combined with GEM treatment. Western blot analysis was applied to detect the expression of certain key regulators of cell apoptosis in PANC-1 cells treated with GEM. shRNA against PPP5C effectively suppressed the proliferation of PANC-1 cells treated with GEM. Additionally, cell cycle analysis indicated that PPP5C knockdown resulted in a higher number of PANC-1 cells treated with GEM in G0/G1 phase arrest. Knockdown of PPP5C increased the expression of associated apoptotic markers, including cleaved caspase 3, poly (ADP-ribose) polymerase and phosphorylated (p)-p53. In addition, the combination of treatment with GEM and PPP5C silencing significantly increased the apoptosis of PANC-1 cells by affecting the expression levels of p-c-Jun N-terminal kinases and p-p38. The present study suggests that PPP5C may be a potential target for the treatment of PC and that it may enhance the gemcitabine sensitivity of PC cells.
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PMID:Knockdown of serine/threonine protein phosphatase 5 enhances gemcitabine sensitivity by promoting apoptosis in pancreatic cancer cells in vitro. 2980 15