Expression of cellular FLICE-inhibitory protein and its association with p53 mutation in colon cance

来源 :World Journal of Gastroenterology | 被引量 : 0次 | 上传用户:baimeng1111
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AIM: To investigate the expression of cellular FLICE (Fas associated death domain-like IL-lbeta-converting enzyme)-inhibitory protein (c-FLIP) and its association with p53 mutation in colon cancer. METHODS: Immunohistochemical staining of c-FLIP and mutant p53 by using specific antibodies was performed by the standard streptavidin-peroxidase technique for 45 colon cancer tissue samples with matched normal tissues. Semi-quantitative reverse transcriptional (RT)-PCR was used to measure c-FLIP mRNA levels, t-test statistical method was used in data analyses. RESULTS: c-FLIP mRNA was expressed in all colon cancer tissues and its level (0.63±0.12) was significantly higher than that in normal tissues (0.38±0.10, P<0.01). Immuno-histochemically, c-FLIP protein was also expressed in all colon cancers (45/45) and 71.1% (32/45) showed an intense immunostaining, in contrast, 93.3% (42/45) of normal colonic mucosa showed positive staining and none of them immunostained intensely. The quantity of c-FLIP protein was significantly higher in cancer tissues than in normal mucosa (7.04±1.20 vs 5.21±0.86, P<0.01). Positive staining of mutant p53 protein was found in 60% (27/45) colon cancers. c-FLIP mRNA level was decreased in p53 positive group compared with p53 negative cancer tissues (0.59±0.13 vs0.69±0.14, P<0.01), but c-FLIP protein had a significantly higher level in p53 positive cancer tissues than in negative ones (7.57±1.30 vs6.25±1.27, P<0.01). CONCLUSION: c-FLIP is specially overexpressed in colon cancers and it might contribute to carcinogenesis of normal colonic mucosa. p53 may exert transcriptional upregulation effects on c-FLI P gene and more potent effects on promoting the degradation of c-FLIP protein. AIM: To investigate the expression of cellular FLICE (Fas associated death domain-like IL-lbeta-converting enzyme) -hibitory protein (c-FLIP) and its association with p53 mutation in colon cancer. METHODS: Immunohistochemical staining of c-FLIP and mutant p53 by using specific antibodies was performed by the standard streptavidin-peroxidase technique for 45 colon cancer tissue samples with matched normal tissues. Semi-quantitative reverse transcriptional (RT) -PCR was used to measure c-FLIP mRNA levels, t-test statistical method was used in data analyzes. RESULTS: c-FLIP mRNA was expressed in all colon cancer tissues and its level (0.63 ± 0.12) was significantly higher than that in normal tissues (0.38 ± 0.10, P <0.01) Immunohistochemically, c-FLIP protein was also expressed in all colon cancers (45/45) and 71.1% (32/45) showed an intense immunostaining, in contrast, 93.3% (42/45) of normal colonic mucosa showed positive staining and none of them immunostained intensely. The quantity of c-FLIP protein was significantly higher in cancer tissues than in normal mucosa (7.04 ± 1.20 vs 5.21 ± 0.86, P <0.01). Positive staining of mutant p53 protein was found in 60% (27/45) mRNA level was decreased in p53 positive group compared with p53 negative cancer tissues (0.59 ± 0.13 vs 0.69 ± 0.14, P <0.01), but c-FLIP protein had a significantly higher level in p53 positive cancer tissues than in negative ones ± 1.30 vs 6.25 ± 1.27, P <0.01). CONCLUSION: c-FLIP is specially overexpressed in colon cancers and it might contribute to carcinogenesis of normal colonic mucosa. P53 may exert transcriptional upregulation effects on c-FLI P gene and more potent effects on promoting the degradation of c-FLIP protein.
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