Hong Xia

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

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Publications (3)3.63 Total impact

  • Bo Su · Jian Su · Hui He · Youhua Wu · Hong Xia · Xi Zeng · Wenxiang Dai · Xiaohong Ai · Hui Ling · Hao Jiang · Qi Su ·
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    ABSTRACT: Diallyl disulfide (DADS) is characterized as an effective agent for the prevention and therapy of cancer, however, mechanisms regarding its anticancer effects are not fully clarified. In the present study, we compared the protein expression profile of gastric cancer MGC-803 cells subjected to DADS treatment with that of untreated control cells to explore potential molecules regulated by DADS. Using proteomic approaches, we identified 23 proteins showing statistically significant differences in expression, including 9 upregulated and 14 downregulated proteins. RT-PCR and western blot analysis confirmed that retinoid-related orphan nuclear receptor α (RORα) and nM23 were increased by DADS, whereas LIM kinase-1 (LIMK1), urokinase-type plasminogen activator receptor (uPAR) and cyclin-dependent kinase-1 (CDK1) were decreased. DADS treatment and knockdown of uPAR caused suppression of ERK/Fra-1 pathway, downregulation of urokinase-type plasminogen activator (uPA), matrix metalloproteinase-9 (MMP-9) and vimentin, and upregulation of tissue inhibitor of metalloproteinase-3 (TIMP-3) and E-cadherin, concomitant with inhibition of cell migration and invasion. Moreover, knockdown of uPAR potentiated the effects of DADS on MGC-803 cells. These data demonstrate that downregulation of uPAR may partially be responsible for DADS-induced inhibition of ERK/Fra-1 pathway, as well as cell migration and invasion. Thus, the discovery of DADS‑induced differential expression proteins is conducive to reveal unknown mechanisms of DADS anti‑gastric cancer.
    Oncology Reports 03/2015; 33(5). DOI:10.3892/or.2015.3859 · 2.30 Impact Factor
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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.
    Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas / Sociedade Brasileira de Biofisica ... [et al.] 03/2010; 43(3):271-8. DOI:10.1590/S0100-879X2010007500004 · 1.01 Impact Factor
  • Hui LING · Li-Feng LU · Ling WEN · Jie HE · Hui TAN · Hong XIA · Qi SU ·
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    ABSTRACT: Chk1 and Chk2 play major role in cell cycle checkpoint signaling pathway, which are mainly involved in G2/M cell cycle checkpoint signal transduction. Firstly, the siRNA targeting at Chk1 or Chk2 gene was transfected into human gastric cancer BGC823 cells for 24 h before 15 mg/L DADS was added. Then, the mRNA and protein expression of Chk1 or Chk2 was detected by Real-time PCR and Western-blot respectively. Cell cycle rates and expressions of CDC25C and cyclinB1 were determined by FCM and Western blot respectively. The results showed that the Chk1 or Chk2 expression was inhibited in Chk1 or Chk2 siRNA-transfected group, in which the Chk1 or Chk2 expression at mRNA level was reduced 84.7% and 69.0% respectively and the protein expression of Chk1 or Chk2 was reduced 73.4% and 78.5% respectively as compared with that in empty control group (P < 0.05). Then it was investigated whether Chk1 and Chk2 proteins could influence cell cycle regulation by knocking down their expressions in BGC823 cells. Further investigation revealed that inhibition of the Chk1 expression in Chk1 siRNA transfected group cut down the proportion of the cells in G2/M phase from 58.1% to 10.4% in BGC823 cells after 24 h induced by DADS (P < 0.05). While inhibition of the Chk2 expression in Chk2 siRNA transfected group had little effect on G2/M arrest after treatment with DADS (P > 0.05). Western blot showed that although DADS decreased expression of CDC25C and cyclinB1 in untransfected cells, inhibition of expression of CDC25C and cyclinB1 treated by DADS was blocked by Chk1 gene silence (P < 0.05). On the contrary, Chk2 gene silence can not do so. These results suggest Chk1 gene silence could abrogate G2/M arrest induced by DADS in BGC823 cell line, and Chk1/CDC25C/cyclinB1 pathway was involved at the G2/M arrest induced by DADS.
    Progress in Biochemistry and Biophysics 02/2010; 37(2):184-189. DOI:10.3724/SP.J.1206.2009.00469 · 0.32 Impact Factor