Nuclear factor I/B promotes colorectal cancer cell proliferation, epithelial-mesenchymal transition and 5-fluorouracil resistance.
Nuclear factor I/B promotes colorectal cancer cell proliferation, epithelial-mesenchymal transition and 5-fluorouracil resistance.
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核因子 I/B 促进结直肠癌细胞增殖、上皮间质转化和 5-氟尿嘧啶耐药。
DOI：
10.1111/cas.13833
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发表时间：
2019-01
期刊：
影响因子：
5.7
通讯作者：
Shu X
中科院分区：
文献类型：
--
作者：
Liu Z;Chen J;Yuan W;Ruan H;Shu Y;Ji J;Wu L;Tang Q;Zhou Z;Zhang X;Cheng Y;He S;Shu X
核因子I/B（NFI B）是一种广泛研究的参与肿瘤进展的转录因子;然而，关于NFI B在结直肠癌（CRC）中的研究有限。在我们的研究中，Western blot和RT-PCR分析显示NFIB在CRC组织和细胞系中过表达，这与我们的生物信息学分析结果一致。NFIB的表达与结直肠癌的TNM分期密切相关。NFIB促进细胞增殖和迁移，抑制细胞凋亡。同时，我们发现NFIB在体内加速异种移植肿瘤的生长。此外，NFIB减弱了CRC细胞对5-氟尿嘧啶（5-FU）的敏感性。NFIB通过上调snail表达诱导上皮-间质转化（EMT），这伴随着E-钙粘蛋白和Zo-1表达的降低和波形蛋白表达的增加。由于Akt通路在CRC进展中起着重要作用，我们研究了NFIB和Akt通路在细胞增殖和迁移中是否存在相关性。我们的结果表明，NFIB通过激活Akt通路促进细胞增殖并增加5-FU抗性。总之，我们的研究结果表明，NFIB通过上调snail表达诱导CRC细胞的EMT，并通过激活Akt通路促进细胞增殖和5-FU耐药性。
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.
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影响因子：
28.2
作者：
Mirabello L;Koster R;Moriarity BS;Spector LG;Meltzer PS;Gary J;Machiela MJ;Pankratz N;Panagiotou OA;Largaespada D;Wang Z;Gastier-Foster JM;Gorlick R;Khanna C;de Toledo SR;Petrilli AS;Patiño-Garcia A;Sierrasesúmaga L;Lecanda F;Andrulis IL;Wunder JS;Gokgoz N;Serra M;Hattinger C;Picci P;Scotlandi K;Flanagan AM;Tirabosco R;Amary MF;Halai D;Ballinger ML;Thomas DM;Davis S;Barkauskas DA;Marina N;Helman L;Otto GM;Becklin KL;Wolf NK;Weg MT;Tucker M;Wacholder S;Fraumeni JF Jr;Caporaso NE;Boland JF;Hicks BD;Vogt A;Burdett L;Yeager M;Hoover RN;Chanock SJ;Savage SA
通讯作者：
Savage SA
影响因子：
4
作者：
Jordà, M;Olmeda, D;Fabra, A
通讯作者：
Fabra, A
影响因子：
--
作者：
Wu N;Jia D;Ibrahim AH;Bachurski CJ;Gronostajski RM;MacPherson D
通讯作者：
MacPherson D
影响因子：
254.7
作者：
Torre, Lindsey A.;Bray, Freddie;Jemal, Ahmedin
通讯作者：
Jemal, Ahmedin
影响因子：
11.1
作者：
Fane ME;Chhabra Y;Hollingsworth DEJ;Simmons JL;Spoerri L;Oh TG;Chauhan J;Chin T;Harris L;Harvey TJ;Muscat GEO;Goding CR;Sturm RA;Haass NK;Boyle GM;Piper M;Smith AG
通讯作者：
Smith AG