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Radiosensitizing effects of miR-101 on HeLa cancer cells and underlying mechanism / 中华放射医学与防护杂志
Chinese Journal of Radiological Medicine and Protection ; (12): 888-892, 2016.
Article in Chinese | WPRIM | ID: wpr-505422
ABSTRACT
Objective To study the effects of microRNAl01 (miR-101)on radiosensitization of human uterine cervix cancer HeLa cells and underlying mechanism.Methods HeLa cells were divided into three groups including blank control,miRNA negative control and miR-101 transfection group.The cells were irradiated by 160 kVp X-ray generated from a linear accelerator at a dose rate of 1.15 Gy/min.Real-time quantitative PCR (qRT-PCR) was used to detect the expression of miR-101.The clonogenic survival assay was applied to evaluate the effect of miR-101 on radiosensitization of HeLa cells.γ-H2AX immunofluorescence and Western blot assays were performed to observe DNA double-strand breaks and the protein expressions of ATM and DNA-PKcs of HeLa cells,respectively.Results Compared with the negative control group,the expression of miR-101 was significantly increased in the HeLa cells at 48 h after transfection with miR-101 mimic,and the survival of HeLa cells over expression of miR-101 was significantly reduced(t =10.75,P < 0.05).The miR-101 had remarkable radiosensitive effect on HeLa cells(F =7.72,P <0.05) with a SERD0 of 1.29.Moreover,over-expression of miR-101 could inhibit the repair of DNA damage induced by irradiation.Compared with the control group,the protein expressions of ATM and DNA-PKcs were significantly decreased in the HeLa cells over expression of miR-101.Conclusions Over-expressions of miR-101 could inhibit cell growth and enhance radiosensitivity of HeLa cells by inhibiting the repair of radiation-induced DNA damage.

Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Radiological Medicine and Protection Year: 2016 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Radiological Medicine and Protection Year: 2016 Type: Article