Tumor-suppressive miR-218-5p inhibits cancer cell proliferation and migration via EGFR in non-small cell lung cancer.
Tumor-suppressive miR-218-5p inhibits cancer cell proliferation and migration via EGFR in non-small cell lung cancer.
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抑癌 miR-218-5p 通过 EGFR 在非小细胞肺癌中抑制癌细胞增殖和迁移
DOI：
10.18632/oncotarget.8576
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发表时间：
2016-05-10
期刊：
影响因子：
--
通讯作者：
Chen X
中科院分区：
文献类型：
--
作者：
Zhu K;Ding H;Wang W;Liao Z;Fu Z;Hong Y;Zhou Y;Zhang CY;Chen X
Lung cancer remains the leading cause of cancer-related death worldwide, and non-small cell lung cancer (NSCLC) accounts for approximately 80% of lung cancer cases. Recently, microRNAs (miRNAs) have been consistently demonstrated to be involved in NSCLC and to act as either tumor oncogenes or tumor suppressors. In this study, we identified a specific binding site for miR-218-5p in the 3′-untranslated region of the epidermal growth factor receptor (EGFR). We further experimentally validated miR-218-5p as a direct regulator of EGFR. We also identified an inverse correlation between miR-218-5p and EGFR protein levels in NSCLC tissue samples. Moreover, we demonstrated that miR-218-5p plays a critical role in suppressing the proliferation and migration of lung cancer cells probably by binding to EGFR. Finally, we examined the function of miR-218-5p in vivo and revealed that miR-218-5p exerts an anti-tumor effect by negatively regulating EGFR in a xenograft mouse model. Taken together, the results of this study highlight an important role for miR-218-5p in the regulation of EGFR in NSCLC and may open new avenues for future lung cancer therapies.
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影响因子：
10.6
作者：
Kumar M;Ernani V;Owonikoko TK
通讯作者：
Owonikoko TK
影响因子：
8.4
作者：
Nicholson, RI;Gee, JMW;Harper, ME
通讯作者：
Harper, ME
DOI：
10.1083/jcb.201208082
发表时间：
2012-10-29
期刊：
The Journal of cell biology
影响因子：
--
作者：
Lindow M;Kauppinen S
通讯作者：
Kauppinen S
DOI：
10.1073/pnas.0702387104
发表时间：
2007-08-07
影响因子：
11.1
作者：
Franovic, Aleksandra;Gunaratnam, Lakshman;Lee, Stephen
通讯作者：
Lee, Stephen
影响因子：
11.1
作者：
Iorio, Marilena V.;Croce, Carlo M.
通讯作者：
Croce, Carlo M.