NFIB functions as an oncogene in estrogen receptor-positive breast cancer and is regulated by miR-205-5p
NFIB functions as an oncogene in estrogen receptor-positive breast cancer and is regulated by miR-205-5p
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NFIB 在雌激素受体阳性乳腺癌中充当癌基因，并受 miR-205-5p 调节
DOI：
10.1016/j.prp.2020.153236
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发表时间：
2020-12-01
影响因子：
2.8
通讯作者：
Hong, Yeting
中科院分区：
文献类型：
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作者：
Chen, Hanxiao;Yu, Chong;Hong, Yeting
核因子I/B（NFIB）是一个重要的转录因子，在癌症进展中起着关键作用。在本研究中，我们发现雌激素受体（ER）阳性乳腺癌组织中NFIB蛋白水平与匹配的邻近非癌组织相比显著上调，而NFIB mRNA表达水平无明显失调。同样，er阳性乳腺癌细胞系MCF7表达NFIB蛋白水平较高，而mRNA水平没有明显上调。功能实验表明，NFIB能促进MCF-7细胞周期进程，促进细胞增殖，抑制细胞凋亡。此外，我们探索了NFIB作为miR-205-5p靶基因的分子机制。最后，我们发现miR-205-5p在er阳性乳腺癌中显著下调，并具有相反的eff；NFIB对乳腺癌细胞的影响。综上所述，本研究突出了NFIB作为er阳性乳腺癌的致癌基因的分子机制，在乳腺癌中受到miR-205-5p的负调控。
Nuclear factor I/B(NFIB) is a prominent transcription factor that plays a critical role in cancer progression. In this study, we found that the protein level of NFIB was significantly upregulated in estrogen receptor (ER) positive breast cancer tissues compared to matched adjacent noncancerous tissues while the NFIB mRNA expression level was not obviously dysregulated. Similarly, ER-positive breast cancer cell line, MCF7 express a high protein level of NFIB, while the mRNA level is not significantly upregulated. The function assays indicated that NFIB promoted MCF-7 cell cycle progression, cell proliferation and suppressed apoptosis in vitro. Furthermore, we explored the molecular mechanisms of NFIB as a target gene of miR-205-5p. Finally, we found that miR-205-5p was significantly downregulated in ER-positive breast cancer, and had the opposite eff ;ects on breast cancer cells compared with NFIB. Taken together, this study highlighted the molecular mechanisms of NFIB as an oncogene in ER-positive breast cancer, which was negatively regulated by miR-205-5p in breast cancer.