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Clinical Research
Correlation between JAK-STAT signal pathway and the development of human rectal cancer
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Abstract:
Objective: To study the possible role for the JAK-STAT signaling pathway in the pathogenesis of rectal cancer. Methods: Cancerous and non-cancerous (control) tissue specimens were collected at surgical resection from 50 rectal cancer patients and 50 non-rectal cancer patients, respectively, who were admitted to our hospital between May, 2013 and May, 2014. Levels of STAT3, p-STAT3 and the two major protein molecules, cyclin D1 and Bcl2, downstream of the JAK-STAT signal pathway in these clinical specimens were assessed by Western blotting analysis and were analyzed statistically for their correlations with the clinical pathological features of the patients. To further evaluate the influence of STAT3 on rectal cancer cell growth, the proliferative activity and invasion ability of colonic carcinoma Colo320 cells after siRNA-mediated silencing of the STAT3 gene was assessed by MTT Transwell migration assays, respectively. Results： Levels of STAT3 were significantly higher in rectal cancer specimens than in non-cancerous control specimens ( P <0.01), so were levels of p-STAT3, cyclin D1 and Bcl2 ( P <0.05). STAT3 protein levels in cancerous specimens were significantly correlated with the differentiation degree and lymphatic metastasis of rectal cancer ( P <0.05), but not with the tumor size ( P >0.05). STAT3 silencing resulted in significant decreases in Colo320 cell proliferation, invasion and metastasis ( P <0.05). Conclusion: STAT3 is involved in the proliferation, invasion and metastasis of colorectal cancer through a JAK-STAT signaling-dependent mechanism and thus may serve as a potential therapeutic target for colorectal cancer.
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