Open AccessNuclear factor I/B promotes colorectal cancer cell proliferation, epithelial‐mesenchymal transition and 5‐fluorouracil resistance
Author(s) -
Liu ZhengYi,
Chen JinHuang,
Yuan WenZheng,
Ruan HaiLong,
Shu Yan,
Ji JinTong,
Wu Liang,
Tang Qiang,
Zhou ZiLi,
Zhang XuDan,
Cheng YiFeng,
He ShuYa,
Shu XiaoGang
Publication year - 2019
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/cas.13833
Subject(s) - cancer research , epithelial–mesenchymal transition , cell growth , vimentin , protein kinase b , colorectal cancer , biology , cancer , medicine , signal transduction , metastasis , immunology , microbiology and biotechnology , immunohistochemistry , genetics
Nuclear factor I/B ( NFIB ) is a widely studied transcription factor that participates in tumor progression; nevertheless, studies on NFIB in colorectal cancer ( CRC ) are limited. In our study, Western blot and RT ‐ PCR analyses showed that NFIB was overexpressed in CRC tissues and cell lines, which was consistent with our bioinformatic analysis results. Furthermore, NFIB expression was closely related to the TNM stage of CRC . NFIB promoted cell proliferation and migration and inhibited cell apoptosis in vitro. Meanwhile, we discovered that NFIB accelerated xenograft tumor growth in vivo. In addition, NFIB weakened the sensitivity of CRC cells to 5‐fluorouracil (5‐ FU ). NFIB induced epithelial‐mesenchymal transition ( EMT ) by upregulating snail expression, which was accompanied by decreased E‐cadherin and Zo‐1 expression and increasedd Vimentin expression. Because the Akt pathway plays an important role in CRC progression, we examined whether there was a correlation between NFIB and the Akt pathway in cell proliferation and migration. Our results showed that NFIB promoted cell proliferation and increased 5‐ FU resistance by activating the Akt pathway. In summary, our findings suggested that NFIB induced EMT of CRC cells via upregulating snail expression and promoted cell proliferation and 5‐ FU resistance by activating the Akt pathway.