MiR-101 sensitizes human nasopharyngeal carcinoma cells to radiation by targeting stathmin 1.
MiR-101 sensitizes human nasopharyngeal carcinoma cells to radiation by targeting stathmin 1.
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miR-101 通过靶向 stathmin 1 使人鼻咽癌细胞对辐射敏感。
DOI：
10.3892/mmr.2015.3221
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发表时间：
2015-05
影响因子：
3.4
通讯作者：
Yuan Y
中科院分区：
文献类型：
--
作者：
Sun Q;Liu T;Zhang T;Du S;Xie GX;Lin X;Chen L;Yuan Y
放射抗性仍然是治疗鼻咽癌（NPC）患者的主要问题。更好地了解参与诱导辐射抗性的机制可能会提供改善NPC患者对治疗的反应的策略。本研究旨在探讨microRNA（miR）-101对鼻咽癌细胞辐射抗性的影响。miR-101表达水平分析表明miR-101在NPC细胞系中下调。此外，miR-101的异位表达抑制了细胞增殖，并增强了NPC细胞的放射敏感性。Stathmin 1（STMN 1）被证实是miR-101的直接功能靶点，参与鼻咽癌细胞的存活、辐射抗性和辐射诱导的自噬。总之，本研究的结果表明，所鉴定的miR-101/STMN 1通路有助于阐明人NPC的辐射抗性机制，并且它可能代表潜在的治疗靶点。
Radioresistance remains a major problem in the treatment of patients suffering from nasopharyngeal carcinoma (NPC). A better understanding of the mechanisms involved in the induction of radioresistance may provide strategies to improve NPC patients’ response to therapy. The present study aimed to investigate the effect of microRNA (miR)-101 on the radioresistance of NPC cells. Analysis of miR-101 expression levels indicated that miR-101 was downregulated in NPC cell lines. Furthermore, ectopic expression of miR-101 suppressed cell proliferation and enhanced radiosensitivity of NPC cells. Stathmin 1 (STMN1) was additionally verified as a direct functional target of miR-101, which was found to be involved in cell viability, radioresistance and radiation-induced autophagy of NPC cells. In conclusions, the results of the present study suggested that the identified miR-101/STMN1 pathway contributed to the elucidation of the mechanisms of radioresistance in human NPC and that it may represent a potential therapeutic target.
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影响因子：
6
作者：
Zhang, Jinqiang;Han, Chang;Wu, Tong
通讯作者：
Wu, Tong
来自FFPE组织的高miR-21表达与结肠癌中辅助化疗的生存不良和对辅助化疗的反应有关。
影响因子：
6.4
作者：
Oue, Naohide;Anami, Katsuhiro;Schetter, Aaron J.;Moehler, Markus;Okayama, Hirokazu;Khan, Mohammed A.;Bowman, Elise D.;Mueller, Annett;Schad, Arno;Shimomura, Manabu;Hinoi, Takao;Aoyagi, Kazuhiko;Sasaki, Hiroki;Okajima, Masazumi;Ohdan, Hideki;Galle, Peter R.;Yasui, Wataru;Harris, Curtis C.
通讯作者：
Harris, Curtis C.
影响因子：
3.8
作者：
Schee K;Boye K;Abrahamsen TW;Fodstad Ø;Flatmark K
通讯作者：
Flatmark K
影响因子：
3.7
作者：
Wang R;Wang HB;Hao CJ;Cui Y;Han XC;Hu Y;Li FF;Xia HF;Ma X
通讯作者：
Ma X
影响因子：
2.2
作者：
GREEN, LM;READE, JL;WARE, CF
通讯作者：
WARE, CF