Long non-coding RNA PVT1 predicts poor prognosis and induces radioresistance by regulating DNA repair and cell apoptosis in nasopharyngeal carcinoma.
Long non-coding RNA PVT1 predicts poor prognosis and induces radioresistance by regulating DNA repair and cell apoptosis in nasopharyngeal carcinoma.
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长链非编码RNA PVT1通过调节鼻咽癌DNA修复和细胞凋亡来预测不良预后并诱导放射抗性
DOI:
10.1038/s41419-018-0265-y
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发表时间:
2018-02-14
影响因子:
9
通讯作者:
Li G
中科院分区:
文献类型:
--
作者:
He Y;Jing Y;Wei F;Tang Y;Yang L;Luo J;Yang P;Ni Q;Pang J;Liao Q;Xiong F;Guo C;Xiang B;Li X;Zhou M;Li Y;Xiong W;Zeng Z;Li G
The long non-coding RNA, plasmacytoma variant translocation 1 (PVT1), is highly expressed in a variety of tumors, and is believed to be a potential oncogene. However, the role and mechanism of action of PVT1 in the carcinogenesis and progression of nasopharyngeal carcinomas (NPCs) remains unclear. In this study, for the first time, we have discovered that PVT1 shows higher expression in NPCs than in normal nasopharyngeal epithelial tissue, and patients with NPCs who show higher expression of PVT1 have worse progression-free and overall survivals. Additionally, we observed that the proliferation of NPC cells decreased, and their rate of apoptosis increased; these results indicated that the knockdown of PVT1 expression in the NPC cells induced radiosensitivity. Further, we have shown that the knockdown of PVT1 expression can induce apoptosis in the NPC cells by influencing the DNA damage repair pathway after radiotherapy. In general, our study shows that PVT1 may be a novel biomarker for prognosis and a new target for the treatment of NPCs. Additionally, targeting PVT1 may be a potential strategy for the clinical management of NPC and for the improvement of the curative effect of radiation in NPCs.
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影响因子:
51.1
作者:
Chen, Lei;Hu, Chao-Su;Ma, Jun
通讯作者:
Ma, Jun
影响因子:
4.3
作者:
Cui, Fengmei;Fan, Rong;Zhou, Ping-Kun
通讯作者:
Zhou, Ping-Kun
影响因子:
11.2
作者:
Feng, Xue-Ping;Yi, Hong;Xiao, Zhi-Qiang
通讯作者:
Xiao, Zhi-Qiang
影响因子:
3.3
作者:
Fan, SQ;Ma, J;Li, GY
通讯作者:
Li, GY
影响因子:
56.9
作者:
Canman, CE;Lim, DS;Siliciano, JD
通讯作者:
Siliciano, JD