Radiation induces premature chromatid separation via the miR-142-3p/Bod1 pathway in carcinoma cells

doi:10.18632/oncotarget.11080

	Radiation induces premature chromatid separation via the miR-142-3p/Bod1 pathway in carcinoma cells
	Li, Xiaoman 3,4,5; Wang, Jufang3,4 ; Hu, Burong1,2,3,4 ; Chen, Yaxiong3,4 ; Ren, Zhenxin3,4 ; Du, Yarong3,4 ; Pan, Dong 3,4,5
刊名	ONCOTARGET
	2016-09-13
卷号	7 页码:60432-60445
关键词	radiation premature chromatid separation miR-142-3p Bod1 radiosensitivity
ISSN号	1949-2553
DOI	10.18632/oncotarget.11080
英文摘要	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.
资助项目	National Natural Science Foundation of China[U1432121] ; National Natural Science Foundation of China[31170803] ; National Key Scientific Instrument and Equipment Development Project of China[2012YQ03014210]
WOS关键词	PROTEIN PHOSPHATASE 2A ; INDUCED GENOMIC INSTABILITY ; STRAND BREAK REPAIR ; IONIZING-RADIATION ; CANCER CELLS ; INDUCED APOPTOSIS ; CERVICAL-CANCER ; MECHANISMS ; PROLIFERATION ; EXPRESSION
WOS研究方向	Oncology ; Cell Biology
语种	英语
出版者	IMPACT JOURNALS LLC
WOS记录号	WOS:000387153900126
资助机构	National Natural Science Foundation of China ; National Key Scientific Instrument and Equipment Development Project of China
内容类型	期刊论文
源URL	[http://119.78.100.186/handle/113462/43665]
专题	近代物理研究所_生物物理研究室近代物理研究所_空间辐射生物研究室
通讯作者	Hu, Burong
作者单位	1.Soochow Univ, Collaborat Innovat Ctr Radiat Med, Jiangsu Higher Educ Inst, Suzhou, Jiangsu, Peoples R China 2.Soochow Univ, Sch Radiol & Interdisciplinary Sci RAD X, Suzhou, Jiangsu, Peoples R China 3.Chinese Acad Sci, Key Lab Heavy Ion Radiat Biol & Med, Lanzhou, Peoples R China 4.Chinese Acad Sci, Inst Modern Phys, Key Lab Space Radiobiol Gansu Prov, Lanzhou, Peoples R China 5.Univ Chinese Acad Sci, Beijing, Peoples R China
推荐引用方式 GB/T 7714	Li, Xiaoman,Wang, Jufang,Hu, Burong,et al. Radiation induces premature chromatid separation via the miR-142-3p/Bod1 pathway in carcinoma cells[J]. ONCOTARGET,2016,7:60432-60445.
APA	Li, Xiaoman.,Wang, Jufang.,Hu, Burong.,Chen, Yaxiong.,Ren, Zhenxin.,...&Pan, Dong.(2016).Radiation induces premature chromatid separation via the miR-142-3p/Bod1 pathway in carcinoma cells.ONCOTARGET,7,60432-60445.
MLA	Li, Xiaoman,et al."Radiation induces premature chromatid separation via the miR-142-3p/Bod1 pathway in carcinoma cells".ONCOTARGET 7(2016):60432-60445.