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Articles by M Gao
Total Records ( 4 ) for M Gao
  B Li , X Chu , M Gao and W. Li

The aim of this study was to investigate the pro-apoptotic mechanism of C-phycocyanin (C-PC)-mediated photodynamic therapy (PDT) in a murine tumor model and cultured MCF-7 cells. The mice were divided into four groups: control, He–Ne laser radiation, C-PC treatment, and C-PC treatment + He–Ne laser radiation. The effects of C-PC and/or laser on immune organs, immunocyte proliferation, tumor genesis, and apoptosis-related proteins expressions were investigated by immunohistochemistry, in situ hybridization, MTT, electron microscope, western blot, and immunofluorescence assay. The results showed that He–Ne laser treatment alone showed marginal effects. In C-PC-treated mice, the weight of immune organs, proliferation of immunocytes, and expression of pro-apoptotic Fas protein were increased, whereas the tumor weight and the expressions of anti-apoptotic proteins (NF-B and P53) and CD44 mRNA were comparatively decreased. In vitro, C-PC was able to inhibit MCF-7 cell proliferation and cause ultrastructural changes including microvilli loss, formation of membrane blebs, and chromatin condensation. Moreover, C-PC treatment could activate caspase-9 expression, induce cytochrome c release, and downregulate Bcl-2 expression. When combined with He–Ne laser irradiation, the effects of C-PC treatment were further enhanced. Facilitating the apoptosis signals transduction and finally leading to the apoptosis of MCF-7 cells may be the mechanism of the anti-tumor activities of C-PC-mediated PDT.

  H Wang , A Zhao , L Chen , X Zhong , J Liao , M Gao , M Cai , D. H Lee , J Li , D Chowdhury , Y. g Yang , G. P Pfeifer , Y Yen and X. Xu

Human Rap1-interacting protein 1 (RIF1) contributes to the ataxia telangiectasia, mutated-mediated DNA damage response against the dexterous effect of DNA lesions and plays a critical role in the S-phase checkpoint. However, the molecular mechanisms by which human RIF1 conquers DNA aberrations remain largely unknown. We here showed that inhibition of RIF1 expression by small interfering RNA led to defective homologous recombination-mediated DNA double-strand break repair and sensitized cancer cells to camptothecin or staurosporine treatment. RIF1 underwent caspase-dependent cleavage upon apoptosis. We further found that RIF1 was highly expressed in human breast tumors, and its expression status was positively correlated with differentiation degrees of invasive ductal carcinoma of the breast. Our results suggest that RIF1 encodes an anti-apoptotic factor required for DNA repair and is a potential target for cancer treatment.

  R Zhao , J. F DeCoteau , C.R Geyer , M Gao , H Cui and A. G. Casson

To evaluate loss of imprinting (LOI) and expression of the IGF2 gene in matched esophageal normal and adenocarcinoma tissues, we studied a prospective cohort of 77 patients who underwent esophageal resection between 1998 and 2003. IGF2 imprinting status was determined by reverse transcription–polymerase chain reaction (PCR) following ApaI digestion, and quantitative PCR was used to evaluate IGF2 expression, which was correlated with clinicopathologic findings, disease-free and overall survival. In total, 32% (14/44) of informative tissues showed loss of IGF2 imprinting, with a strong correlation between the tumor and normal esophageal epithelia (Kappa = 0.89, P < 0.01). Normal epithelia with LOI had increased expression of IGF2 [median: 2.91, 95% confidence interval (CI): 0.93–5.06] compared with imprinted normal epithelia (median: 1.13, 95% CI: 0.85–1.39) (P = 0.03). In contrast, tumors with LOI had significantly reduced IGF2 expression (median: 1.87, 95% CI: 0.53–5.21) compared with normally imprinted tumors (median: 6.79, 95% CI: 3.39–15.89) (P = 0.016). Patients below the age of 65 years with normally imprinted tumors had significantly reduced 5 year disease-free survival (DFS) (24%) compared with patients whose tumors had LOI for IGF2 (55%) (P = 0.03). Cox regression analysis showed that IGF2 overexpression was associated with significantly reduced disease-free survival (P = 0.04). We conclude that in a subgroup of younger patients, loss of IGF2 imprinting was associated with improved outcome following esophageal resection. Expression of IGF2 in esophageal adenocarcinoma and normal esophageal epithelia depended on imprinting status and tissue type, suggesting novel molecular regulatory mechanisms in esophageal tumorigenesis.

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