IFNγ induces Bcl3 expression by JAK1/STAT1/p65 signaling, resulting in increased IL-8 expression in ovarian cancer cells

被引：5
作者：
Gaire, Bijaya [1 ]
Padmanabhan, Sveta [1 ]
Zou, Yue [1 ]
Uddin, Mohammad M. [1 ]
Reddy, Suprataptha U. [1 ]
Vancurova, Ivana [1 ]
机构：
[1] St Johns Univ, Dept Biol Sci, 8000 Utopia Pkwy, New York, NY 11439 USA
来源：
FEBS OPEN BIO | 2023年 / 13卷 / 08期
关键词：
Bcl3; IFN & gamma; interleukin-8; JAK1; ovarian cancer; STAT1; NF-KAPPA-B; 1ST-LINE TREATMENT; CLASSICAL HODGKIN; ONCOPROTEIN BCL-3; ENCODES; ACTIVATION; PATHWAY; P50; INTERLEUKIN-8; TRANSCRIPTION;
D O I：
10.1002/2211-5463.13624
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
We have recently shown that IFN?, produced during cancer therapy, induces expression of the Bcl3 proto-oncogene in ovarian cancer (OC) cells, resulting in their increased proliferation, migration, and invasion, but the mechanisms are unknown. Here, we demonstrate that the IFN?-induced Bcl3 expression is dependent on JAK1 and STAT1 signaling, and on p65 NF?B. Furthermore, the IFN?-induced Bcl3 expression is associated with an increased occupancy of Ser-727 phosphorylated STAT1 and acetylated histone H3 at the Bcl3 promoter. Our data indicate that Bcl3 promotes expression of the pro-inflammatory chemokine interleukin-8 (IL-8) in OC cells. These findings identify Bcl3 as a novel target of IFN?/JAK1/STAT1 signaling and suggest that targeting the JAK1/STAT1 pathway may suppress IFN?-induced Bcl3 expression in OC.
引用
收藏
页码：1495 / 1506
页数：12
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