Abstract |
The aim of this study was to evaluate the changes in radiosensitivity of radioresistant esophageal cancer cells (TE-1R) after disruption of replication protein A (RPA) expression and to explore the potential mechanism. A radioresistant human esophageal cancer cell line TE-1R was established by treating TE-1 cells with the radiation. Then, siRPA1 or -2 was transfected to TE-1R cells. The untransfected group (control) and nonsense short interfering RNA ( siRNA) transfected group (NC) were used as controls. To investigate the radiosensitivity changes of TE-1R cells, the dose-survival curve was established by colony-forming assay, and the cell cycle distribution was measured by flow cytometry. (1) Comparing with control and NC groups, the protein expression of RPA1 and -2 decreased significantly 48 h after siRPA1 or -2 transfection. (2) The D 0, D q, and SF2 values reduced from 2.09, 1.70, and 0.85 in NC group to 1.67, 0.71, and 0.44 and 1.82, 0.89, and 0.51 in siRNA1 and siRPA2 transfected groups, respectively. The D q sensitization enhancement ratios (SERDq) were 2.39 and 1.91 in siRNA1 and siRPA2 transfected groups, respectively. (3) The G2/M arrest was significantly caused by siRPA1 or -2 transfection as compared with that in the NC group (t value was 2.827, 2.853, p < 0.05). Post transcriptional silencing of RPA1 or -2 via RNAi can enhance the radiosensitivity of human esophageal cancer cells TE-1R, and the potential mechanism may be related to the inhibition of post-radiation sublethal damage repair and the halted cell cycle progression at G2/M phase. Therefore, RPA may become a new target for radiosensitization enhancement in esophageal cancer.
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Authors | Zhao Di, Sun Sanyuan, Lu Hong, Yu Dahai |
Journal | Cell biochemistry and biophysics
(Cell Biochem Biophys)
Vol. 70
Issue 2
Pg. 887-91
(Nov 2014)
ISSN: 1559-0283 [Electronic] United States |
PMID | 24789547
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- RNA, Small Interfering
- Replication Protein A
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Topics |
- Cell Line, Tumor
- DNA Damage
(genetics)
- Esophageal Neoplasms
(pathology)
- G2 Phase Cell Cycle Checkpoints
(genetics, radiation effects)
- Gene Expression Regulation, Neoplastic
(genetics, radiation effects)
- Gene Knockdown Techniques
- Humans
- M Phase Cell Cycle Checkpoints
(genetics, radiation effects)
- RNA, Small Interfering
(genetics)
- Radiation Tolerance
(genetics, radiation effects)
- Replication Protein A
(deficiency, genetics)
- Time Factors
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