1. Center for Research and Technology of Precision Medicine, College of Life Sciences and Oceanography, Shenzhen University, Shenzhen, Guangdong 518055, P. R. China.
2. Laboratory of Molecular Pathology, Shantou University Medical College, Shantou, Guangdong 515041, P. R. China.
3. Pathology Laboratory, Shantou University Medical College, Cancer Hospital, Shantou, Guangdong 515041, P. R. China.
*Equal contribution as first author
Currently, it reported that TAF1L gene mutation is found in a number of carcinomas, but its pathophysiological function has not been well studied. We focused on investigating expressive levels of TAF1L gene and protein in esophageal squamous cell carcinoma (ESCC) with two tissue microarrays, forty fresh paired ESCC and paracancer samples using immunohistochemistry, real-time PCR or Western blot in this study. Furthermore, we executed TAF1L silence with siRNA in ESCC cell lines to evaluate effects of TAF1L expression on cell proliferation, migration and invasion of ESCC via CCK-8, wound healing and transwell chamber assays. Moreover, key proteins related to ESCC development were also analyzed by Western blot. Results from this study showed that the expression of TAF1L mRNA and protein in ESCC tissues were significantly higher than that in matched paracancer tissues. However, its abnormal expression was not associated with other clinic features, such as the age, gender and pathological grade, except of TNM-N stage. Furthermore, the proliferation, migration and invasion of ESCC cells were inhibited after TAF1L gene silencing. As a consequence, the expression of c-Myc and phosphorylated Akt in esophageal squamous cell line after TAF1L-siRNA treatment were inversely decreased, while p53 was increased significantly, compared those to control group. Taken together, the results from this study suggest that TAF1L gene might be served as an oncogene, and its overexpression could accelerate to the tumorigenesis of ESCC via promoting the malignant cell proliferation and tumor metastasis.
Keywords: TAF1L, ESCC, tumorigenesis, cell proliferation, tumor metastasis.