H. Xia

University of South China, Heng-nan, Hunan, China

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Publications (4)1.01 Total impact

  • H. Tan · X. Ji · L. Yi · H. Xia · J. Wang · J. He · H. Ling · Q. Su
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    ABSTRACT: Objective: To investigate the role of MAPKs, phosphatidylinositol 3-kinase-Akt pathway, and the Bcl-2 family proteins in diallyl disulfide (DADS)-induced apoptosis. Methods: Flow cytometry analysis was used to detect apoptotic cells. Western blot analysis of the expression of phospho-MAPKs ( ERK and p38), phospho-AKT, and the Bcl-2 family proteins was used to elucidate the possible mechanisms of DADS-induced apoptosis. Results: DADS induced significant apoptosis, which exhibited a dose-dependent and time-dependent response (P < 0.05). DADS inhibited the ERK/MAPK and the PI3K/AKT pathways, followed by the downregulation of the anti-apoptotic factor Mcl-1 and the upregulation of the pro-apoptotic factor Bax. The P38/MAPK pathways were activated and did not affect the expression of Mcl-1 and Bax. Small interfering RNA-mediated downregulation of Mcl-1 significantly sensitized the leukemia cells to DADS-induced apoptosis. Conclusion: These results clearly demonstrate that the PI3K/AKT and MAPK signaling path¬way is involved in the induction of apoptosis by DADS and it is mediated by the downregulation of Mcl-1 in human HL-60 cells.
    No preview · Article · Jun 2011
  • H. Ling · L. Wen · Z.-W. Chen · Z.-F. Li · H. Xia · Q. Su
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    ABSTRACT: OBJECTIVE: To investigate the effect of Chk1/2 gene silencing on the cell viability of human gastric cancer cell line MGC803, and explore the role of Chk1 and Chk2 in cell cycle. METHODS: The siRNA targeting at Chk1 or Chk2 gene was transfected into MGC803 cells. The protein expression of Chk1 and Chk2 was detected by Western blot. Cell viability and cell cycle rates were determined by MTT assay and FCM. RESULTS: The gray values of Chk1 and Chk2 protein were 0.09±0.04 and 0.12±0.01, both o which were lower than those of untransfected group (0.39±0.09) and liposome transfected group (0.38±0.17, P<0.05). However, there was no difference between untransfected group and liposome transfected group (P = 0.458). The Chk1 and Chk2 expression at protein level in Chk1 and Chk2 siRNA-transfected group was reduced 85.0% and 83.4% respectively. The lack of Chk1 expression resulted in decreased cellular proliferation activity, and its inhibition rate was 38.0% (t = 26.767, P<0.05). However, The lack of Chk2 expression had no effect on proliferation of MGC803 cells (t = 6.098, P>0.05). Further investigation revealed that the cell cycle was delayed at the G0/G1 phase with the especially remarkable arrest occurring in the cases of Chk1 siRNA, but without apoptosis. The lack of Chk2 expression was not involved in cell cycle. CONCLUSIONS: The proliferation of human gastric cancer MGC803 cells are inhibited by Chk1 gene silence. G0/G1 arrest is involved in the inhibition effect under the lack of Chk1 expression.
    No preview · Article · Apr 2010 · Chinese Journal of Cancer Prevention and Treatment
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    H Ling · L Wen · X X Ji · Y L Tang · J He · H Tan · H Xia · J G Zhou · Q Su
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    ABSTRACT: Diallyl disulfide (DADS) inhibits growth and induces cell cycle G2/M arrest in human gastric cancer MGC803 cells. In this study, 15 mg/L DADS exerted similar effects on growth and cell cycle arrest in human gastric cancer BGC823 cells. Due to the importance of cell cycle redistribution in DADS-mediated anti-carcinogenic effects, we investigated the role of checkpoint kinases (Chk1 and Chk2) during DADS-induced cell cycle arrest. We hypothesized that DADS could mediate G2/M phase arrest through either Chk1 or Chk2 signal transduction pathways. We demonstrated that DADS induced the accumulation of phosphorylated Chk1, but not of Chk2, and that DADS down-regulated Cdc25C and cyclin B1. The expression of mRNA and total protein for Chkl and Chk2 was unchanged. Chk1 is specifically phosphorylated by ATR (ATM-RAD3-related gene). Western blot analysis showed that phospho-ATR was activated by DADS. Taken together, these data suggest that cell cycle G2/M arrest, which was associated with accumulation of the phosphorylated forms of Chk1, but not of Chk2, was involved in the growth inhibition induced by DADS in the human gastric cancer cell line BGC823. Furthermore, the DADS-induced G2/M checkpoint response is mediated by Chk1 signaling through ATR/Chk1/Cdc25C/cyclin B1, and is independent of Chk2.
    Preview · Article · Mar 2010 · Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas / Sociedade Brasileira de Biofisica ... [et al.]
  • H. Ling · X. Ji · L. Wen · H. Xia · H. Tan · J. He · H. Tang · L. Dong · Q. Su
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    ABSTRACT: Objective: Cell cycle has recently become more appealing as a new target of anti-carcinogenic agent. Diallyl disulfide (DADS) inhibits growth and induces cell cycle G2/M arrest in human gastric cancer BGC823 cells. Cell division cycle protein 25C (Cdc25C) and CyclinB1 expression are involved in G2/M arrest. However, mechanisms of G2/M arrest are not yet fully understood. The aim of this study was to elucidate the mechanism of cell cycle G2/M arrest in human gastric cancer BGC823 cells induced by DADS. Methods: The expression of Chk1 and Chk2 mRNA associated with cell cycle arrest of BGC823 cells after the induction with DADS for 1 or 2 days was detected by RT-PCR. The protein expression of cycle-related proteins ATM-RAD3-related gene (ATR), checkpoint kinase1 (Chk1), checkpoint kinase 2 (Chk2), P-ATR, P-Chk1 and P-Chk2 was measured by Western blot. Interaction between Chk1/2 and Cdc25C was analyzed by immunoprecipitation. Results: After the cells were treated with 15 mg/L DADS for 1 or 2 days, the expression of Chk1 and Chk2 mRNA was not significantly different from that in untreated cells (P>0.05). Western blot analysis showed that the expression of total Chk1 and Chk2 treated with 15 mg/L DADS was not significantly different from that in untreated cells. But phospho-Chk1 showed a significant increase after stimulation with 15 mg/L DADS for 2h to 12h and continued to increase gradually as time went on (P<0.05). Pnospho-Chk2 showed a weak expression and a weaker expression after stimulation with DADS, but the changes were not statistically significant (P>0.05). Addition of 15 mg/L DADS to BGC823 cells for 15 min to 120 min resulted in an increase in phospho-ATR expression, whereas no changes were found in ATR expression (P<0.05). The Chk1 Ab increasingly precipitated Cdc25C in BGC823 cells treated with DADS (P<0.05). In contrast, Chk2 Ab failed to change precipitation with Cdc25C by DADS (P>0.05). Conclusion: Activation of Chk1 was involved in cell cycle G2/M arrest in BGC823 cells treated with DADS. Cell cycle G2/M arrest by DADS is associated with phosphorylation of several cell cycle regulatory proteins including ATR and Chk1 which regulate expression of Cdc25C.
    No preview · Article · Feb 2010