X-ray inhibits FUT4-mediated proliferation in A549 cells by downregulating SP1 expression
Jin-Xiao Liang1, Wei Gao2, Wei-Tian Wei1
1Department of Oncological Surgery, Cancer Hospital of the University of Chinese Academy of Sciences, Zhejiang Cancer Hospital, China.
Objective:
To identify the mechanism of down-regulation of Lewis Y antigen caused by X-ray irradiation.
Methods:
The present original research study was conducted at Zhejiang University City College, Hangzhou, Republic of China, from 2020 to 2022. Western blotting, Co-immunoprecipitation (CO-IP), electrophoretic mobility shift assay and Cell Counting Kit-8 (CCK8) were performed to confirm the effect of X-ray irradiation on A549 cell proliferation and its mechanism. Data was analysed using Statistical Package for Social Sciences (SPSS) 11.5.
Results:
The expressions of fucosyltransferase IV and Lewis Y were decreased after X-ray irradiation, thus inhibiting the proliferation of A549 lung cancer cells. Deoxyribonucleic acid damage caused by the irradiation caused higher level of poly- adenosinediphosphate-ribosylated Specific Protein 1(SP1), and translocation of SP1 from the nucleus, decreasing the expression of fucosyltransferase IV and Lewis Y.
Conclusion:
There was a significant role of glycosylation in radiation therapy for lung cancer.
Insights
X-ray irradiation down-regulates Lewis Y antigen expression in lung cancer cells by affecting fucosyltransferase IV and SP1. This mechanism inhibits A549 cell proliferation, highlighting glycosylation's role in radiation therapy.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Lewis Y antigen is a key biomarker in various cancers.
- Understanding antigen modulation during radiation therapy is crucial for treatment optimization.
Purpose of the Study:
- To elucidate the mechanism by which X-ray irradiation down-regulates Lewis Y antigen expression.
- To investigate the impact of X-ray irradiation on A549 lung cancer cell proliferation and its underlying molecular pathways.
Main Methods:
- Western blotting and Co-immunoprecipitation (CO-IP) were used to analyze protein expression and interactions.
- Electrophoretic mobility shift assay and Cell Counting Kit-8 (CCK8) assessed DNA damage and cell proliferation.
- Statistical analysis was performed using SPSS 11.5.
Main Results:
- X-ray irradiation decreased the expression of fucosyltransferase IV and Lewis Y antigen in A549 lung cancer cells.
- Irradiation-induced DNA damage led to increased poly-adenosinediphosphate-ribosylated Specific Protein 1 (SP1) levels.
- Translocation of SP1 from the nucleus resulted in reduced expression of fucosyltransferase IV and Lewis Y.
Conclusions:
- X-ray irradiation inhibits A549 lung cancer cell proliferation through the down-regulation of Lewis Y antigen.
- The mechanism involves DNA damage, increased SP1, and subsequent decreased expression of fucosyltransferase IV and Lewis Y.
- Glycosylation plays a significant role in the efficacy of radiation therapy for lung cancer.
