Radiation induces premature chromatid separation via the miR-142-3p/Bod1 pathway in carcinoma cells
Metrics: PDF 429 views | HTML 317 views | ?
Dong Pan1,2, Yarong Du1, Zhenxin Ren1, Yaxiong Chen1, Xiaoman Li1,2, Jufang Wang1, Burong Hu1,3
1Key Laboratory of Heavy Ion Radiation Biology and Medicine of Chinese Academy of Sciences & Key Laboratory of Space Radiobiology of Gansu Province, Institute of Modern Physics, Chinese Academy of Sciences, Lanzhou, China
2University of Chinese Academy of Sciences, Beijing, China
3Collaborative Innovation Center of Radiation Medicine of Jiangsu Higher Education Institutions and School for Radiological and Interdisciplinary Sciences (RAD-X), Soochow University, Suzhou, Jiangsu, China
Burong Hu, email: email@example.com
Keywords: radiation, premature chromatid separation, miR-142-3p, Bod1, radiosensitivity
Received: January 06, 2016 Accepted: July 26, 2016 Published: August 5, 2016
Radiation-induced genomic instability plays a vital role in carcinogenesis. Bod1 is required for proper chromosome biorientation, and Bod1 depletion increases premature chromatid separation. MiR-142-3p influences cell cycle progression and inhibits proliferation and invasion in cervical carcinoma cells. We found that radiation induced premature chromatid separation and altered miR-142-3p and Bod1 expression in 786-O and A549 cells. Overexpression of miR-142-3p increased premature chromatid separation and G2/M cell cycle arrest in 786-O cells by suppressing Bod1 expression. We also found that either overexpression of miR-142-3p or knockdown of Bod1 sensitized 786-O and A549 cells to X-ray radiation. Overexpression of Bod1 inhibited radiation- and miR-142-3p-induced premature chromatid separation and increased resistance to radiation in 786-O and A549 cells. Taken together, these results suggest that radiation alters miR-142-3p and Bod1 expression in carcinoma cells, and thus contributes to early stages of radiation-induced genomic instability. Combining ionizing radiation with epigenetic regulation may help improve cancer therapies.
Primary Contact _
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.