Int J Biol Sci 2020; 16(7):1180-1193. doi:10.7150/ijbs.41148
TAF1L promotes development of oral squamous cell carcinoma via decreasing autophagy-dependent apoptosis
1. Center for Research and Technology of Precision Medicine, College of Life Sciences and Oceanography, Shenzhen University, Shenzhen, Guangdong, China.
2. Key Laboratory of Optoelectronic Devices and Systems of Ministry of Education and Guangdong Province, College of Optoelectronic Engineering, Shenzhen University, Shenzhen, Guangdong, China.
3. Key Laboratory of Shaanxi Province for Craniofacial Precision Medicine Research, College of Stomatology, Xi'an Jiaotong University. Xi'an, Shanxi, China
Wang D, Qi H, Zhang H, Zhou W, Li Y, Li A, Liu Q, Wang Y. TAF1L promotes development of oral squamous cell carcinoma via decreasing autophagy-dependent apoptosis. Int J Biol Sci 2020; 16(7):1180-1193. doi:10.7150/ijbs.41148. Available from http://www.ijbs.com/v16p1180.htm
This study focused on investigating the relationships of TAF1L expression and clinical features or pathological stages of oral squamous cell carcinoma (OSCC), and its potential roles of TAF1L on OSCC development. Western blot and immunohistochemical staining were used to detect TAF1L expression in OSCC tissues and cells. Effects of TAF1L on OSCC cells in vitro were examined by cell proliferation assay, wound healing assay, transwell chamber assay, flow cytometry analysis and siRNA technique. Cellular key proteins related to cell autophagy and apoptosis were evaluated by Western blot and immunofluorescent staining. Moreover, functions of TAF1L on OSCC process were observed in nude mouse model. Testing results showed that expression of TAF1L protein was higher in OSCC tissues than that in normal oral epithelial or paracancerous tissues. Additionally, the level of TAF1L protein expression was upregulated in OSCC cell lines, compared to that in normal oral epithelial cells. Furthermore, cell proliferation, migration, autophagy and apoptosis were modulated post siRNA-TAF1L treatment in vitro. Especially, TAF1L knockdown-induced apoptotic activation on OSCC cells could be rescued by autophagic activator (Rapamycin). Moreover, that overexpression of TAF1L protein could promote the growth of OSCC cell xenografts was confirmed in nude mouse model. Taken together, it suggests that TAF1L may facilitate OSCC cells to escape cell apoptosis via autophagic activation for enhancing OSCC development.
Keywords: TAF1L, OSCC, apoptosis, autophagy, siRNA