A novel β-catenin signaling pathway activated by IL-1β leads to the onset of epithelial–mesenchymal transition in breast cancer cells

Pérez-Yépez, Eloy Andrés; Ayala-Sumuano, Jorge-Tonatiuh; Lezama, Ruth; Meza, Isaura

doi:10.1016/j.canlet.2014.08.015

Cited by 60 publications

(67 citation statements)

References 43 publications

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“…We found that in 3D cultures, TcES promoted the reorganization of the actin cytoskeleton in RKO cells, altering the cell morphology and forming colonospheres. As previously reported in other cancer models, tumor cell reorganization is associated with a low grade of aggressiveness; thus, our data suggest a regulatory effect of TcES on signals associated with migration and invasiveness.…”

Section: Discussionsupporting

confidence: 89%

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Helminth‐derived molecules inhibit colitis‐associated colon cancer development through NF‐κB and STAT3 regulation

Callejas

Mendoza

Villamar-Cruz

et al. 2019

Intl Journal of Cancer

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Inflammation is currently considered a hallmark of cancer and plays a decisive role in different stages of tumorigenesis, including initiation, promotion, progression, metastasis and resistance to antitumor therapies. Colorectal cancer is a disease widely associated with local chronic inflammation. Additionally, extrinsic factors such as infection may beneficially or detrimentally alter cancer progression. Several reports have noted the ability of various parasitic infections to modulate cancer development, favoring tumor progression in many cases and inhibiting tumorigenesis in others. The aim of our study was to determine the effects of excreted/secreted products of the helminth Taenia crassiceps (TcES) as a treatment in a murine model of colitis-associated colon cancer (CAC). Here, we found that after inducing CAC, treatment with TcES was able to reduce inflammatory cytokines such as IL-1β, TNF-α, IL-33 and IL-17 and significantly attenuate colon tumorigenesis. This effect was associated with the inhibition of signal transducer and activator of transcription 3 and nuclear factor kappa-light-chainenhancer of activated B cells (NF-κB) phosphorylation. Furthermore, we determined that TcES interfered with LPS-induced NF-κB p65 activation in human colonic epithelial cell lines in a Raf-1 proto-oncogene-dependent manner. Moreover, in threedimensional cultures, TcES promoted reorganization of the actin cytoskeleton, altering cell morphology and forming colonospheres, features associated with a low grade of aggressiveness. Our study demonstrates a remarkable effect of Additional Supporting Information may be found in the online version of this article.

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Section: Discussionsupporting

confidence: 89%

“…NF‐κB also influences the activity of the Wnt/β‐catenin signaling pathway, which could alter the actin cytoskeleton, conferring cancer cells with a migration ability . We found that in 3D cultures, TcES promoted the reorganization of the actin cytoskeleton in RKO cells, altering the cell morphology and forming colonospheres.…”

Section: Discussionmentioning

confidence: 80%

Helminth‐derived molecules inhibit colitis‐associated colon cancer development through NF‐κB and STAT3 regulation

Callejas

Mendoza

Villamar-Cruz

et al. 2019

Intl Journal of Cancer

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“…Recent studies have been demonstrated that MSCs exosomes have therapeutic effects in tissue repair in liver, skin and heart [31][32][33][34][35][36]. A number of studies have examined the role of MSC-derived exosomes in cancer development, metastasis, drug resistance and progression of cancer [37][38][39][40].…”

Section: Discussionmentioning

confidence: 99%

“…Lastly, molecular analysis of exosomal mRNA indicates that some exosomes carry a specific selection of mRNAs which are associated with, amongst other things, signaling pathways such as the PI3K/Akt signaling pathway [26]. The PI3K/Akt signaling pathway plays a crucial role in the regulation of gene expression, which is involved in the proliferation, migration and metastasis of tumor cells [31]. The protein kinase B (PKB), also known as Akt, is a serine/ threonine-specific protein kinase which is encoded by the genes Akt1, Akt2 and Akt3 [32].…”

Section: Discussionmentioning

confidence: 99%

Adipose-Derived Stem Cells (ASC) Communicate with Residual Breast Cancer Cells

Reinkens¹,

Pm²,

Bucan³

2017

J Mol Genet Med

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“…IL‐18 has been shown to control caspase 8‐mediated apoptosis in gastric cancer cells [34]. In breast cancer, IL‐1β induces malignant cell proliferation by inducing nuclear translocation of β‐catenin [35]. Additionally, IL‐1β has been shown to regulate angiogenesis in several settings [36,37] as well as immune suppression mechanisms, by inducing myeloid‐derived suppressor cells [38].…”

Section: Is There a Role For Inflammasome Activation In Cancer Immunomentioning

confidence: 99%

Role of inflammasome activation in tumor immunity triggered by immune checkpoint blockers

Segovia

Russo

Girotti

et al. 2020

Clinical and Experimental Immunology

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Immune checkpoint blockers improve the overall survival of a limited number of patients among different cancers. Identifying pathways that influence the immunological and clinical response to treatment is critical to improve the therapeutic efficacy and predict clinical responses. Recently, a key role has been assigned to innate immune mechanisms in checkpoint blockade-driven anti-tumor responses. However, inflammatory pathways can both improve and impair anti-tumor immunity. In this review, we discuss how different inflammatory pathways, particularly inflammasome activation, can influence the clinical outcome of immune checkpoint blockers. Inflammasome activation may reinforce anti-tumor immunity by boosting CD8 + T cell priming as well as by enhancing T helper type 17 (Th17) responses. In particular, we focus on the modulation of the cation channel transmembrane protein 176B (TMEM176B) and the ectonucleotidase CD39 as potential targets to unleash inflammasome activation leading to reinforced anti-tumor immunity and improved efficacy of immune checkpoint blockers. Future studies should be aimed at investigating the mechanisms and cell subsets involved in inflammasome-driven anti-tumor responses.

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A novel β-catenin signaling pathway activated by IL-1β leads to the onset of epithelial–mesenchymal transition in breast cancer cells

Cited by 60 publications

References 43 publications

Helminth‐derived molecules inhibit colitis‐associated colon cancer development through NF‐κB and STAT3 regulation

Helminth‐derived molecules inhibit colitis‐associated colon cancer development through NF‐κB and STAT3 regulation

Adipose-Derived Stem Cells (ASC) Communicate with Residual Breast Cancer Cells

Role of inflammasome activation in tumor immunity triggered by immune checkpoint blockers

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