FOXP1 inhibits pancreatic cancer growth by transcriptionally regulating IRF1 expression

被引:6
作者
Wang, Le [1 ,2 ]
Luo, Ping [3 ]
Yang, Zhiwen [4 ]
Zhong, Xiaoming [1 ,5 ]
Ji, Changxue [6 ]
机构
[1] Nanchang Univ, Med Coll, Grad Sch, Nanchang, Jiangxi Provinc, Peoples R China
[2] Jiangxi Canc Hosp, Jiangxi Clin Res Ctr Canc, Sci Res Sect, Nanchang, Jiangxi Provinc, Peoples R China
[3] Nanchang Third Hosp, Dept Breast Surg, Nanchang, Peoples R China
[4] Songjiang Dist Cent Hosp, Dept Pharm, Shanghai, Peoples R China
[5] Jiangxi Canc Hosp, Jiangxi Clin Res Ctr Canc, Dept Oncol Radiotherapy, Nanchang, Jiangxi, Peoples R China
[6] Songjiang Dist Cent Hosp, Dept Vasc Intervent Radiol, Shanghai, Peoples R China
关键词
B-CELL LYMPHOMA; POOR-PROGNOSIS; OVEREXPRESSION; SURVIVAL; SUBSET; GENE; BETA;
D O I
10.1371/journal.pone.0280794
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
FOXP1, known as a Forkhead-box (FOX) family protein, plays an important role in human tumorigenesis. However, the function and molecular mechanism of FOXP1 in pancreatic cancer (PC) remain unclear. Here, we report that PC patients with FOXP1 overexpression had a higher survival rate compared to patients with low- FOXP1 expression. Additionally, high expression of FOXP1 can markedly inhibit the growth of pancreatic cancer in vivo and in vitro, whereas low expression of FOXP1 effectively promoted the tumorigenesis. Mechanistically, FOXP1 could directly bind the IRF1 promoter, which triggered the transcriptional activity of IRF1. Taken together, FOXP1 suppressed PC growth via IRF1-dependent manner, serving as a potential prognostic biomarker for patients with PC.
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页数:14
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