The Research On The Role Of STAT3Signal Pathways In Colonic Cancer Implanted Tumor Lymphangiogenesis In Homologous Mice

Objective:To study effectively the change in Lymphangiogenesis in implanted colonic cancer in homologous mice and the role of signal transduction and transcription activated factor3(STAT3) signal pathways in Lymphangiogenesis, and anti-tumor Lymphangiogenesis effectively.Methods:The BALB/c mice model of implanted colonic cancer was established using BALB/c mice tumor cell lines CT-26. Mice were divided into three groups randomly (blank control group, DMSO group and inhibitor group:STAT3inhibitor WP1066plus DMSO). The expression of p-STAT3, VEGF-C was tested by immunohistochemistry staining. The number of Lymphangiogenesis marked by anti-podoplanin monoclonal antibody was also investigated. The mRNA transcription level of STAT3. VEGF-C. PODOPLANIN was determined by real-time quantitative PCR using fluorescence. The relationship was analyzed and compared with relevant data from the implanted colonic tumor in BALB/c mice.Results:There is no significant difference in tumor size between the blank group and DMSO group (p>0.05). However, the tumor size in the inhibitor group was significantly lower than in other two groups (p<0.05).The protein expression of p-STAT3、VEGF-C have no significant difference between blank and DMSO group (p>0.05). However, there was significantly lower level in inhibitor group than other two groups (p<0.05).There is no significant difference in Lymphangiogenesis level between blank and DMSO group (p>0.05). However, a significantly lower level was noted in the inhibitor group compared to the other two groups (p<0.05).There is no significant difference in the mRNA transcription level of STAT3、 VEGF-C、PODOPLANIN in tumor tissues of the blank group compared to the DMSO group (p>0.05). However, there was a significantly lower level was recorded in the inhibitor group compared to the other two groups (p<0.05).There is positive correlation of mRNA transcription and expression of STAT3to VEGF-C in implanted colonic tumor (P<0.05).Both the mRNA transcription and expression level of STAT3and VEGF-C have positive correlation to those of PODOPLANIN (P<0.05). The same correlation is also observed for the number of Lymphangiogenesis.Conclusions:Implanted colonic cancer model can be established in homologous BALB/c mice use mice Colonic cancer cell lines CT26. Lymphangiogenesis and the regulation effect of STAT3/VEGF-C/PODOPLANIN signal pathways can be observed and analyzed in the implanted tumor model. Implanted colonic cancer model achieved100%tumor formation, suggesting that CT26may have effect in tumor immune escape. Inhibition of STAT3signal pathways may develop into a promising treatment in colon cancer therapy.