Publications (3)0 Total impact
Article: Glivec enhances the down-regulated cytotoxicity of adriamycin in acquired tamoxifen-resistant MCF-7 cell line.[show abstract] [hide abstract]
ABSTRACT: To study the alteration of bax, bcl-2, p170 expressing and the second effect on the adriamycin (ADR) induced cytotoxicity in acquired tamoxifen (TAM)-resistant MCF-7 cell line. The bax, bcl-2, p170 protein expressions were detected by flow cytometry respectively, as well as the content of intracellular ADR. The in vitro adenosine triphosphate tumor chemosensitivity assay (ATP-TCA) was performed to evaluate the cytotoxicity of ADR, and also the effect of Glivec on the cytotoxicity of ADR. The percentages of bax, bcl-2 expressions in the acquired TAM resistant MCF-7 were down-regulated from 53.17+/-1.45% to 28.70+/-1.41% (P <0.01), 41.53+/-2.17% to 37.87+/-1.86% P >0.05 respectively, the p170 was up-regulated from 27.43+/-2.16% to 32.13+/-1.31% (P <0.05), after a 16-week-treatment with 1 x 10(-7) mol/L TAM. Accordingly, the chemosensitivity and the fluorescence intensity of intracellular ADR declined, both of them can be significantly reversed by 10 microg/ml Glivec. The acquired TAM resistant MCF-7 accompanied with a declined ADR cytotoxicity, down-regulation of bcl-2/bax-induced apoptosis and up-regulation of p170-induced drug efflux may had a synergic devotion. Glivec may enhance the cytotoxicity of ADR on the acquired TAM-resistant MCF-7 cell line.Di 1 jun yi da xue xue bao = Academic journal of the first medical college of PLA 07/2003; 23(7):731-3.
Article: [Molecular mechanism of antisense glycosyltransferase oligonucleotide inhibiting human gliomas cell line SWO-38].[show abstract] [hide abstract]
ABSTRACT: It was reported that Globo series glycoshingolipids have relationship to many human cancers, and alpha 1, 4-galactosyltransferase(alpha 1, 4Gal-T) oligonucleotide is the specific glycosyltransferase for the synthesis of Globo series glycoshingolipids. This study was designed to evaluate the effects of antisense alpha 1, 4Gal-T oligonucleotide on human gliomas cell line SWO-38. SWO-38 glioma cells were reacted with 10 mumol/L antisense alpha 1, 4Gal-T oligonucleotide for 72 hours by means of lipofectin transfection. The growth inhibition was detected by colony-forming unit assay. DNA fragmentation was examined by flow cytometric analysis(FCM) and agarose gel eletrophoresis. The expressions of fas, p53, bax, and bcl-2 protein were determined by flow cytometric analysis (FCM). Antisense alpha 1, 4Gal-T oligonucleotide signifantly inhibited cell growth (P < 0.01), induced the apoptosis (P < 0.05), downregulated expression of bcl-2 protein (P < 0.01) and upregulated expressions of fas and bax protein (P < 0.01), but did not influence p53 expression in glioma cell line SWO-38. Antisense alpha 1, 4Gal-T oligonucleotide can significantly inhibit proliferation and induce apoptosis in human gliomas cell line SWO-38, which maybe due to the interactions of fas, bax, and bcl-2.Ai zheng = Aizheng = Chinese journal of cancer 10/2002; 21(10):1095-9.
Article: [Effects of lipofectin-mediated alpha1,4Gal T antisense oligonucleotide on human glioma cell line SWO-38].[show abstract] [hide abstract]
ABSTRACT: To study the effects of alpha1,4Gal T antisense oligonucleotide mediated by lipofectin on human glioma cell line SWO-38. SWO38 glioma cells were exposed to 10 micromol/L alpha1,4Gal T antisense oligonucleotide for 72 h by means of lipofectin transfection, and the growth inhibition of the cells was detected by colony-forming unit assay. Analysis of DNA fragmentation was performed with flow cytometry (FCM) and agarose gel eletrophoresis with Fas protein expression determined by FCM. alpha1,4Gal T antisense oligonucleotide significantly inhibited the growth of glioma cells (P<0.01) and induced apoptosis in SWO-38 cells (P<0.05). Marked up-regulation of Fas protein expression was observed in response to the treatment (P<0.01). alpha1,4Gal T antisense oligonucleotide can significantly inhibit SWO-38 cell proliferation and induce cellular apoptosis, the mechanism of which may involve up-regulated Fas expression.Di 1 jun yi da xue xue bao = Academic journal of the first medical college of PLA 04/2002; 22(4):299-302.