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10.3748/wjg.v21.i23.7197

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suck abstract from ncbi


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pmid26109806
      World+J+Gastroenterol 2015 ; 21 (23 ): 7197-207
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  • Paeoniflorin inhibits human gastric carcinoma cell proliferation through up-regulation of microRNA-124 and suppression of PI3K/Akt and STAT3 signaling #MMPMID26109806
  • Zheng YB ; Xiao GC ; Tong SL ; Ding Y ; Wang QS ; Li SB ; Hao ZN
  • World J Gastroenterol 2015[Jun]; 21 (23 ): 7197-207 PMID26109806 show ga
  • AIM: To examine the potential anti-tumor activity of paeoniflorin in the human gastric carcinoma cell line MGC-803. METHODS: Cell viability and cytotoxic effects in MGC-803 cells were analyzed using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and lactate dehydrogenase assay, respectively. Cell apoptosis of MGC-803 cells was measured using flow cytometry, DAPI staining assay and caspase-3 activity assay. Quantitative reverse transcription-polymerase chain reaction (RT-PCR) was used to measure the expression of microRNA-124 (miR-124) in response to paeoniflorin. The expression of phosphatidylinositol 3-kinase (PI3K), protein kinase B (Akt), phospho-Akt (p-Akt) and phospho-signal transducer and activator of transcription 3 (p-STAT3) were also measured by quantitative RT-PCR and Western blot analysis in normal, miR-124 and anti-miR-124 over-expressing MGC-803 cells, treated with paeoniflorin. RESULTS: Paeoniflorin was found to inhibit MGC-803 cell viability in a dose-dependent manner. Paeoniflorin treatment was associated with the induction of apoptosis and caspase-3 activity in MGC-803 cells. Paeoniflorin treatment significantly increased miR-124 levels and inhibited the expression of PI3K, Akt, p-Akt and p-STAT3 in MGC-803 cells. Interestingly, the over-expression of miR-124 inhibits PI3K/Akt and phospho-STAT3 expressions in MGC-803 cells. PI3K agonist (IGF-1, 1 ?g/10 ?L) or over-expression of STAT3 reversed the effect of paeoniflorin on the proliferation of MGC-803 cells. Over-expression of anti-miR-124 in MGC-803 cells reversed paeoniflorin-induced up-regulation. CONCLUSION: In summary, the in vitro data suggest that paeoniflorin is a potential novel therapeutic agent against gastric carcinoma, which inhibits cell viability and induces apoptosis through the up-regulation of miR-124 and suppression of PI3K/Akt and STAT3 signaling.
  • |Antineoplastic Agents, Phytogenic/*pharmacology [MESH]
  • |Apoptosis/drug effects [MESH]
  • |Blotting, Western [MESH]
  • |Carcinoma/*drug therapy/enzymology/genetics/pathology [MESH]
  • |Caspase 3/metabolism [MESH]
  • |Cell Line, Tumor [MESH]
  • |Cell Proliferation/*drug effects [MESH]
  • |Cell Survival/drug effects [MESH]
  • |Dose-Response Relationship, Drug [MESH]
  • |Gene Expression Regulation, Neoplastic [MESH]
  • |Glucosides/*pharmacology [MESH]
  • |Humans [MESH]
  • |MicroRNAs/*metabolism [MESH]
  • |Monoterpenes/*pharmacology [MESH]
  • |Phosphatidylinositol 3-Kinase/*metabolism [MESH]
  • |Phosphorylation [MESH]
  • |Proto-Oncogene Proteins c-akt/*metabolism [MESH]
  • |Real-Time Polymerase Chain Reaction [MESH]
  • |STAT3 Transcription Factor/*metabolism [MESH]
  • |Signal Transduction/*drug effects [MESH]
  • |Stomach Neoplasms/*drug therapy/enzymology/genetics/pathology [MESH]
  • |Time Factors [MESH]
  • |Transfection [MESH]


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