Proliferative and invasive effects of inhibitors of kinase 4(P15(ink4b) and P16(ink4a)/CDKN2) gene activation on RKO human colorectal cancer cells / 中华胃肠外科杂志

<p><b>OBJECTIVE</b>To explore the proliferation and invasive effects of inhibitors of kinase 4(INK4)(P15(ink4b) and P16(ink4a)/CDKN2) gene protein activation on RKO human colorectal cell in vivo and in vitro.</p><p><b>METHODS</b>RKO human colorectal cell line was exposed to the specific DNA methyltransferase inhibitor 5-Aza-CdR and INK4(P15(ink4b) and P16(ink4a)/CDKN2) protein expression was detected by Western blotting. Soft agar cloning experiment and Transwell chamber assay were used to detect the proliferative and invasive ability in vitro. Tumorigenicity in nude mice was analyzed in vivo.</p><p><b>RESULTS</b>INK4(P15(ink4b) and P16(ink4a)/CDKN2) protein expression of RKO human colorectal cells after exposure to 1×10(-7), 5×10(-7) and 1×10(-6) mol/L 5-Aza-CdR concentrations(A, B, C groups) were 1.13, 1.38, 1.92 folds and 1.11, 1.45, 2.14 folds compared to positive control group respectively. Soft agar cloning experiment showed the number of cell colony significantly decreased from 36.8±5.1(positive control group) to 32.4±7.2, 21.3±5.4 and 19.5±6.4 (3 experiment groups, all P<0.05) respectively. Transwell chamber assay showed that migrated cell number in positive control group(67.4±7.2) was significantly higher than those of 3 experimental groups(35.3±4.6, 29.5±7.3 and 25.3±6.2, respectively). The tumor volume of metastasis model in nude mice was inhibited in experimental groups, but not significantly lower compared to control group (P>0.05). There were significant differences of tumor weight and inhibition rate between control group and 3 experimental groups in nude mice respectively(all P<0.01).</p><p><b>CONCLUSION</b>INK4(P15(ink4b) and P16(ink4a)/CDKN2) protein activation can inhibit tumor proliferation, migration and suppress the tumor formation ability.</p>

Chondrocyte apoptosis in rabbit temporomandibular joint after anterior disc displacement / 中华口腔医学杂志

<p><b>OBJECTIVE</b>To study the chondrocyte apoptosis in rabbit temporomandibular joint after anterior disc displacement.</p><p><b>METHODS</b>Experimental anterior disc displacement was induced surgically in 20 Japanese rabbits without opening their temporomandibular joint bursas. Histopathologic and apoptotic (TUNEL) analysis was used to evaluate the changes in articular cartilage, disc and synovium.</p><p><b>RESULTS</b>Condyle chondrocyte showed apoptosis most obviously at 1 or 2 weeks after surgery, and apoptotic cells concentrated in proliferative zone and hypertrophic zone. 4 or 6 weeks after surgery, the joint went into a remodelling period.</p><p><b>CONCLUSIONS</b>Chondrocyte apoptosis in temporomandibular joint will be activated after anterior disc displacement, which initiates the remodelling in temporomandibular joint.</p>

Prognostic prediction of PTEN and Her-2 expression in breast cancer / 中国病理生理杂志

AIM: To study the prognositic value of PTEN and Her-2 expression in primary breast cancer.METHODS: 81 breast cancer specimens with 15 years follow-up were obtained from 1989 to 2004.Immunohistochemical methods were used to detect the expression of PTEN and Her-2 in 81 paraffin-embedded specimens.The correlation between expression of PTEN and clinipathological factors was discussed with the Chi-square test.The survival rate analysis results were calculated with Kaplan-meier method.Long-rank test and Cox model by SPSS 10.0 software.RESULTS:(1) PTEN expression significantly affects 5-year and 10-year survival rate of breast cancer(P

Antitumor effect of chlorophyllin in vitro / 中国病理生理杂志

AIM: To study the effect and mechanism of chlorophyllin (CHL) inhibiting HT29 cells. METHODS: IC 50 value and growth curve of HT29 cells were detected with MTT method. Apoptosis was detected with Wright-Giemsa staining, FCM and DNA electrophoresis. Telomerase was detected by PCR-ELISA, and protein and mRNA expression of COX-2 gene were detected through RT-PCR and Western blot. RESULTS: CHL inhibited the growth of HT29 in a dose-dependent manner. CHL blocked HT29 cells in G 1 phase but did not induce apoptosis. Different concentration of CHL inhibits the expression of telomerase and COX-2 in HT29 cells. CONCLUSION: CHL inhibits the growth of HT29 cells by inhibiting the expression of telomerase and COX-2 and blocking cells in G 1 phase. [