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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.

Nuclear factor I/B promotes colorectal cancer cell proliferation, epithelial‐mesenchymal transition and 5‐fluorouracil resistance