miR-365 promotes cutaneous squamous cell carcinoma (CSCC) through targeting nuclear factor I/B (NFIB).
miR-365 promotes cutaneous squamous cell carcinoma (CSCC) through targeting nuclear factor I/B (NFIB).
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miR-365 通过靶向核因子 I/B (NFIB) 促进皮肤鳞状细胞癌 (CSCC)
DOI:
10.1371/journal.pone.0100620
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发表时间:
2014
期刊:
影响因子:
3.7
通讯作者:
Ding Z
中科院分区:
文献类型:
--
作者:
Zhou M;Zhou L;Zheng L;Guo L;Wang Y;Liu H;Ou C;Ding Z
Aberrant expression of microRNAs plays vital roles in tumor development and progression. As transcription factors (TFs) are the critical components of signaling cascades, specific targeting effects of microRNAs to specific TFs may determine the role of microRNAs in different cancers. In this study, we identified Nuclear Factor I/B (NFIB) as one of the targets of miR-365 which was previously verified as an onco-miR in cutaneous squamous cell carcinoma (CSCC). Down-regulation of NFIB was a general feature in both CSCC cell lines and tumors from patients which show drastically up-regulated miR-365 expression levels. The siRNA-based knockdown of NFIB mimic the carcinogenic transformation of normal cells by ectopically expression of miR-365 which indicates depletion of NFIB is necessary for miR-365 to exert its pro-carcinogenic function. NFIB may represent a functional barrier targeted by miR-365 to the development of CSCC. Further studies also discovered a conserved feedback regulatory circuitry formed by NFIB and miR-365 in CSCC development which may be potentially utilized as therapeutic target to improve the clinical CSCC treatment.
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影响因子:
50.3
作者:
Wang H;Garzon R;Sun H;Ladner KJ;Singh R;Dahlman J;Cheng A;Hall BM;Qualman SJ;Chandler DS;Croce CM;Guttridge DC
通讯作者:
Guttridge DC
影响因子:
2.7
作者:
Hsu YC;Osinski J;Campbell CE;Litwack ED;Wang D;Liu S;Bachurski CJ;Gronostajski RM
通讯作者:
Gronostajski RM
影响因子:
3.3
作者:
Guo, Ling;Huang, Zhong-Xi;Ding, Zhen-Hua
通讯作者:
Ding, Zhen-Hua
影响因子:
64.5
作者:
Lewis, BP;Shih, IH;Burge, CB
通讯作者:
Burge, CB
影响因子:
4.7
作者:
Zhou M;Liu W;Ma S;Cao H;Peng X;Guo L;Zhou X;Zheng L;Guo L;Wan M;Shi W;He Y;Lu C;Jiang L;Ou C;Guo Y;Ding Z
通讯作者:
Ding Z