IFNγ induces JAK1/STAT1/p65 NFκB-dependent interleukin-8 expression in ovarian cancer cells, resulting in their increased migration

Padmanabhan, Sveta; Gaire, Bijaya; Zou, Yue; Uddin, Mohammad M.; DeLeon, Daniel; Vancurova, Ivana

doi:10.1016/j.biocel.2021.106093

Cited by 9 publications

(4 citation statements)

References 54 publications

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“…Even though the JAK/STAT pathway is the main mechanism responsible for the expression of ISGs [ 28 , 29 , 30 ], several studies have shown that the IFNγ‐induced expression of NFκB‐dependent genes can be regulated also by p65 NFκB [ 42 , 43 ]. To examine the possibility that the IFNγ‐induced Bcl3 expression in OC cells might be dependent on p65 NFκB, we analyzed the Bcl3 expression in IFNγ‐treated SKOV3 cells transfected with p65 siRNA.…”

Section: Resultsmentioning

confidence: 99%

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

et al. 2023

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We have recently shown that IFNγ, 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 IFNγ‐induced Bcl3 expression is dependent on JAK1 and STAT1 signaling, and on p65 NFκB. Furthermore, the IFNγ‐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 IFNγ/JAK1/STAT1 signaling and suggest that targeting the JAK1/STAT1 pathway may suppress IFNγ‐induced Bcl3 expression in OC.

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Section: Resultsmentioning

confidence: 99%

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

et al. 2023

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“…It induced epithelial mesenchymal transition of OC cells and promoted migration and invasion of cancer cells ( 54 ). IFN-γ had the similar role, inducing IL-8 expression through JAK1/STAT1 signaling and p65 NFκB-mediated, thus helping OC cells to migrate ( 55 , 56 ). In Addition to that, the synergistic effect of IFN-γ/JAK and ERK signaling pathways induced the expression of skin-specific protein suprabasin (SBSN) in OC cells, which reduced the adhesion of cancer cells and made them more resistant to apoptosis of lost nests, aiding OC cells metastasis and stem-cell-like property ( 57 ).…”

Section: The Roles Of Ifns In Ovarian Cancer Immunitymentioning

confidence: 98%

The role of interferons in ovarian cancer progression: Hinderer or promoter?

Liu

Wang

et al. 2022

Front. Immunol.

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Ovarian cancer (OC) is a common gynecologic malignancy with poor prognosis and high mortality. Changes in the OC microenvironment are closely related to the genesis, invasion, metastasis, recurrence, and drug-resistance. The OC microenvironment is regulated by Interferons (IFNs) known as a type of important cytokines. IFNs have a bidirectional regulation for OC cells growth and survival. Meanwhile, IFNs positively regulate the recruitment, differentiation and activation of immune cells. This review summarizes the secretion and the role of IFNs. In particular, we mainly elucidate the actions played by IFNs in various types of therapy. IFNs assist radiotherapy, targeted therapy, immunotherapy and biotherapy for OC, except for some IFN pathways that may cause chemo-resistance. In addition, we present some advances in OC treatment with the help of IFN pathways. IFNs have the ability to powerfully modulate the tumor microenvironment and can potentially provide new combination strategies for OC treatment.

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“…Of course, hyperinsulinemia is not the only mechanistic link between obesity and cancer. Although discussion of these alternative mechanisms is beyond the scope of this review, we acknowledge that insulin-independent mechanisms — for example, lipid peroxidation and metabolism [ 213 ], fibroblast growth factor receptor-1 [ 214 ], creatine [ 215 ], leptin [ 216 ], inflammatory cytokines [ 217 ], and many others which space limitations do not permit us to discuss in any detail ( Figure 4 ) — play a key role in the progression of obesity-associated cancers as well.…”

Section: Hyperinsulinemia As a Therapeutic Target In Animals With Cancermentioning

confidence: 99%

Insulin and cancer: a tangled web

Leitner

Siebel

Akingbesote

et al. 2022

Biochemical Journal

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For a century, since the pioneering work of Otto Warburg, the interwoven relationship between metabolism and cancer has been appreciated. More recently, with obesity rates rising in the U.S. and worldwide, epidemiologic evidence has supported a link between obesity and cancer. A substantial body of work seeks to mechanistically unpack the association between obesity, altered metabolism, and cancer. Without question, these relationships are multifactorial and cannot be distilled to a single obesity- and metabolism-altering hormone, substrate, or factor. However, it is important to understand the hormone-specific associations between metabolism and cancer. Here, we review the links between obesity, metabolic dysregulation, insulin, and cancer, with an emphasis on current investigational metabolic adjuncts to standard-of-care cancer treatment.

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IFNγ induces JAK1/STAT1/p65 NFκB-dependent interleukin-8 expression in ovarian cancer cells, resulting in their increased migration

Cited by 9 publications

References 54 publications

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

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

The role of interferons in ovarian cancer progression: Hinderer or promoter?

Insulin and cancer: a tangled web

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