MiR-124 enhances cell radiosensitivity by targeting PDCD6 in nasopharyngeal carcinoma

被引:0
|
作者
Zhang, Yuqin [1 ]
Zheng, Lin [3 ]
Lin, Shuimiao [4 ]
Liu, Ying [1 ]
Wang, Yiming [1 ]
Gao, Fei [2 ]
机构
[1] Jinan Univ, Affiliated Hosp 1, Dept Radiat Oncol, Guangzhou 510630, Guangdong, Peoples R China
[2] Jinan Univ, Affiliated Hosp 1, Dept Gastroenterol, Guangzhou 510630, Guangdong, Peoples R China
[3] Southern Med Univ, Sch Basic Med Sci, Dept Pathol, Guangzhou, Guangdong, Peoples R China
[4] Southern Med Univ, Nanfang Hosp, Dept Radiat Oncol, Guangzhou, Guangdong, Peoples R China
来源
INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY | 2017年 / 10卷 / 12期
基金
中国国家自然科学基金;
关键词
miR-124; PDCD6; radiosensitivity; NPC; BREAST-CANCER; PROTEIN ALG-2; LUNG-CANCER; MICRORNAS; RADIORESISTANCE; EXPRESSION; DEATH; IDENTIFICATION; RADIOTHERAPY; METASTASIS;
D O I
暂无
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Background: Radiation resistance poses a major clinical challenge in treatment of nasopharyngeal carcinoma (NPC). Studies have shown that the abnormal expression of microRNAs (miRNAs) is associated with radiosensitivity, however, the mechanisms have not been fully elucidated. The aim of this study, therefore, was to investigate whether ectopic expression of miR-124 is correlated with radiosensitivity in NPC. Methods: In this study, the expression level of miR-124 was evaluated in NPC cell lines and patient specimens using quantitative reverse transcription-PCR (Real-time qPCR). Cell radiosensitivity was determined by colony formation assay. Target prediction algorithms and luciferase assay were used to confirm the target of miR-124. Tumor xenograft model was performed to understand the functions of miR-124 in vivo. Results: We found that miR-124 was down-regulated in both NPC specimens and NPC cell lines. Ectopic expression of miR-124 increased radiosensitivity of NPC cells. In vivo assays extended the significance of these results, showing that miR-124 overexpression decreased cell resistance to radiation treatment in tumor xenografts. Furthermore, we identified PDCD6 as a novel direct target of miR-124. Functional studies showed that knockdown PDCD6 enhanced cell radosensitivity to irradiation, and PDCD6 could rescue the effect caused by overexpression of miR-124, indicating that PDCD6 is a functional target of miR-124. Conclusions: MiR-124 enhances cell radiosensitivity by targeting PDCD6, miR-124/PDCD6 axis may facilitate the development of novel targeted therapies for NPC.
引用
收藏
页码:11461 / +
页数:11
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