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BRAF激活的长链非编码RNA促进甲状腺乳头状癌的细胞增殖并激活自噬。

BRAF-activated long non-coding RNA contributes to cell proliferation and activates autophagy in papillary thyroid carcinoma.

作者信息

Wang Yong, Guo Qinhao, Zhao Yan, Chen Jiejing, Wang Shuwei, Hu Jun, Sun Yueming

机构信息

Department of General Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210000, P.R. China.

Department of Obstetrics and Gynecology, Northern Jiangsu Province Hospital, Clinical Medical College, Yangzhou University, Yangzhou, Jiangsu 225001, P.R. China.

出版信息

Oncol Lett. 2014 Nov;8(5):1947-1952. doi: 10.3892/ol.2014.2487. Epub 2014 Aug 28.

Abstract

Long non-coding RNAs (lncRNAs) are novel regulators in cancer biology. BRAF-activated lncRNA (BANCR) is overexpressed in melanoma and has a potential functional role in melanoma cell migration. However, little is known about the role of BANCR in the development of papillary thyroid carcinoma (PTC). In the present study, BANCR expression was examined in six pairs of PTC and matched adjacent normal tissues. The results revealed that BANCR levels were significantly higher in the PTC tissues and PTC IHH-4 cells compared with the normal controls. Knockdown of BANCR in the IHH-4 cells inhibited proliferation and increased apoptosis of the cells . Further investigation of the underlying mechanisms revealed that BANCR markedly activated autophagy. Overexpression of BANCR inhibited apoptosis in the IHH-4 cells, whereas inhibition of autophagy stimulated apoptosis in the BANCR-overexpressed cells. BANCR overexpression also increased cell proliferation and the inhibition of autophagy abrogated BANCR overexpression-induced cell proliferation. In addition, the overexpression of BANCR resulted in an increase in the ratio of LC3-II/LC3-I, a marker for autophagy, while the knockdown of BANCR decreased the ratio of LC3-II/LC3-I. These results revealed that BANCR expression levels are upregulated in PTC. Additionally, BANCR increases PTC cell proliferation, which could activate autophagy.

摘要

长链非编码RNA(lncRNAs)是癌症生物学中的新型调节因子。BRAF激活的lncRNA(BANCR)在黑色素瘤中过表达,并且在黑色素瘤细胞迁移中具有潜在的功能作用。然而,关于BANCR在甲状腺乳头状癌(PTC)发生发展中的作用知之甚少。在本研究中,检测了6对PTC组织及其配对的癌旁正常组织中BANCR的表达。结果显示,与正常对照相比,PTC组织和PTC IHH-4细胞中BANCR水平显著更高。敲低IHH-4细胞中的BANCR可抑制细胞增殖并增加细胞凋亡。对潜在机制的进一步研究表明,BANCR可显著激活自噬。BANCR过表达可抑制IHH-4细胞凋亡,而抑制自噬则可刺激BANCR过表达细胞的凋亡。BANCR过表达还可增加细胞增殖,抑制自噬可消除BANCR过表达诱导的细胞增殖。此外,BANCR过表达导致自噬标志物LC3-II/LC3-I的比例增加,而敲低BANCR则降低了LC3-II/LC3-I的比例。这些结果表明,PTC中BANCR表达水平上调。此外,BANCR可增加PTC细胞增殖,这可能激活自噬。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3a7/4186573/757c1ae06637/OL-08-05-1947-g00.jpg

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