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A Journal on Internal Medicine
Indexed/Abstracted in: BIOSIS Previews, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 1,6
Panminerva Medica 2015 December;57(4):183-9
RPA1 expression in esophageal carcinoma and its influence on radiosensitivity of esophageal carcinoma TE-1 cells
Zhang D. J. 1, Xiang J. 2, Wang X. 1, Wang J. 1, Xiao J. C. 1, Xu W. 1, Xu H. 1, Xin Y. 3, Zhang L. Z. 3, Pei D. S. 4, Zheng J. N. 4, Gu Y. M. 1 ✉
1 Department of Interventional Radiology, Affiliated Hospital of Xuzhou Medical College Xuzhou, Jiangsu, China;
2 Department of Rehabilitation Medicine, Affiliated Hospital of Xuzhou Medical College Xuzhou, Jiangsu, China;
3 Department of Radiotherapy, Affiliated Hospital of Xuzhou Medical College, Xuzhou, Jiangsu, China;
4 Jiangsu Key Laboratory of Biological Cancer Therapy, Xuzhou Medical College, Xuzhou, Jiangsu, China
AIM: To determinate the RPA1 expression in esophageal carcinoma and the paired tumor-adjacent tissue, and to explore the influence of RPA1 on radiosensitivity of esophageal carcinoma TE-1 cells.
METHODS: Firstly, the RPA1 expression of 40 cases esophageal carcinoma and their adjacent tissues were detected by immunohistochemistry. Secondly, The esophageal carcinoma cell subline-radiation resistance model (TE-1R) was constructed by radiation-induction, the RPA1 expression and proliferation activity of TE-1 and TE-1R cells were detected by Western blot and MTT assay respectively. After radiation, the expression of RPA1 and cell apoptosis were detected by Western blot and FACS respectively. Cell clone formation and survival rate were detected by clonogenic assay. Thirdly, Inhibiting RPA1 expression by siRNA in TE-1 cells, the expression of RPA1 was detected by RT-PCR and Western blot, Cell proliferation inhibition ratio and cell apoptosis after radiation were detected by MTT assay and FACS respectively.
RESULTS: The RPA1 expression in esophageal carcinoma was significantly higher than that in the tumor-adjacent tissues, which was associated with tumor invasion and lymph node metastasis. The RPA1 expression in TE-1R cells was higher than that in TE-1 cells, while the proliferation activity of TE-1R cells was lower than that of TE-1 cells, and the apoptosis rate of TE-1R cells after radiation was less than that of TE-1 cells. In addtion, the clone formation and survival rate of TE-1R cells were higher than that of TE-1 cells. Moreover, inhibiting RPA1 expression by siRNA-RPA1 could promoted proliferation inhibition ratio and apoptosis rate of TE-1 cells after radiation.
CONCLUSION: The over-expression of RPA1 in esophageal carcinoma was related with progression and metastasis. Moreover, radiation induced the excessive expression RPA1 in TE-1 cells, and the radiosensitivity of TE-1R cells was less than that of TE-1 cells. Furthermore, inhibiting RPA1 expression could increase radiosensitivity of TE-1 cells. Overall, RPA1 could influence radiosensitivity and might be one important mechanism of radiation resistance in TE-1 cells.