IL-1β induces up-regulation of BIRC3, a gene involved in chemoresistance to doxorubicin in breast cancer cells

Mendoza, Mónica; Romero, Hugo; Fuentes‐Pananá, Ezequiel M.; Ayala-Sumuano, Jorge-Tonatiuh; Meza, Isaura

doi:10.1016/j.canlet.2017.01.005

Cited by 61 publications

(57 citation statements)

References 34 publications

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“…[18] Our results confirm these observations but also demonstrate that IL-1β exerts its tumorigenic effects through regulation of an oncogene. Consistently, IL-1β stimulation leads to upregulation of genes involved in breast cancer cell survival [22] In this study, IL-1β expression was higher in epithelium-derived tumor cells than in CD45 + lymphocytes in ESCC tissues. We speculate that this is not only due to increased lymphocyte infiltration but also because IL-1β production was enhanced, resulting in genetic alterations in tumor cells.…”

Section: Discussionsupporting

confidence: 75%

FRAS1-related extracellular matrix protein 2 drives the progression and poor prognosis of IL-1β-associated esophageal squamous cell carcinoma

Wang¹,

Gu²,

Liu³

et al. 2019

Preprint

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Background Chronic inflammation generates a tumor-supporting microenvironment, but it remains unclear whether and how the persistent inflammation drives genetic abnormalities leading to the occurrence and progression of esophageal squamous cell carcinoma (ESCC). Methods By global RNA-sequncing, we screened genes related to ESCC with stimulation of the pro-inflammatory factor, interleukin (IL)-1β, and identified FRAS1-related extracellular matrix protein (FREM)2 as a oncogene. Flow cytometry was used to detect the expression of IL-1β and its receptor IL-1R1 in fresh ESCC specimens. The interaction between FREM2 and IL-1β signal was examined in vitro and in vivo. Levels of FREM2 and IL-1R1 were determined in ESCC tissue arrays derived from 299 patients, and their correlation with clinical outcomes was analyzed. Results Multiple genes-related to ESCC occurrence and recurrence were elevated when exposed to the persistent stimulation of IL-1β. Among them, FRAS1-related extracellular matrix protein 2 (FREM2) was identified as a new oncogene in ESCC. IL-1β and its receptor IL-1R1 highly expressed in ESCC, especially in tumor cells. FREM2 was induced by IL-1β, and in turn bound to and stabilized IL-1R1, facilitating IL-1β signal transduction. The activation of downstream NK-κB and JNK signals mediated the tumor-promoting effect, while the reduction of FoxP1 was responsible for IL-1β-induced FREM2 transcription. High levels of FREM2 and IL-1R1 synergistically indicated the shorter survival time in patients. Conclusion These results suggest FREM2 is an IL-1β-stimulated oncogene, which as a cofactor of IL1R1 promotes IL-1β-induced ESCC progression. Therapeutic strategies targeting FREM2 is likely to prolong the survival of ESCC patients.

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Section: Discussionsupporting

confidence: 75%

FRAS1-related extracellular matrix protein 2 drives the progression and poor prognosis of IL-1β-associated esophageal squamous cell carcinoma

Wang¹,

Gu²,

Liu³

et al. 2019

Preprint

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“…Total RNA was extracted from colon tissue using an RNA/Protein purification kit (Norgen Biotek Corp, Ontario, Canada). The reactions were performed according to previous reports . The specific primers for all genes are shown in Supporting Information Table S1.…”

Section: Methodsmentioning

confidence: 99%

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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“…However, anandamide-induced degradation of cytoplasmic β-catenin, while CBD relocated β-catenin at the adherens junctions. In both cases the expression of malignant markers in 6D cells was greatly reduced [5,16,17]. In this work, we analyzed the expression of two genes, BIRC3 and TP63, the expression of which was increased by the activation of the IL-1β/IL-1R/β-catenin pathway.…”

Section: Discussionmentioning

confidence: 99%

“…As the above data revealed that addition of CBD to 6D cells caused morphological and molecular changes described in the IL-1β-induced EMT, we investigated if CBD could have a negative effect on the expression of genes and proteins that participate in this process [16,17]. Therefore, qRT-PCR analysis was performed for BIRC3, TP63, and ID1 genes.…”

Section: Cbd Decreased the Expression Of Proteins Related To The Il-1mentioning

confidence: 99%

CBD Reverts the Mesenchymal Invasive Phenotype of Breast Cancer Cells Induced by the Inflammatory Cytokine IL-1β

García-Morales

Castillo

Tapia-Ramı́rez

et al. 2020

IJMS

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Cannabidiol (CBD) has been used to treat a variety of cancers and inflammatory conditions with controversial results. In previous work, we have shown that breast cancer MCF-7 cells, selected by their response to inflammatory IL-1β cytokine, acquire a malignant phenotype (6D cells) through an epithelial–mesenchymal transition (EMT). We evaluated CBD as a potential inhibitor of this transition and inducer of reversion to a non-invasive phenotype. It decreased 6D cell viability, downregulating expression of receptor CB1. The CBD blocked migration and progression of the IL-1β-induced signaling pathway IL-1β/IL-1RI/β-catenin, the driver of EMT. Cannabidiol reestablished the epithelial organization lost by dispersion of the cells and re-localized E-cadherin and β-catenin at the adherens junctions. It also prevented β-catenin nuclear translocation and decreased over-expression of genes for ∆Np63α, BIRC3, and ID1 proteins, induced by IL-1β for acquisition of malignant features. Cannabidiol inhibited the protein kinase B (AKT) activation, a crucial effector in the IL-1β/IL-1RI/β-catenin pathway, indicating that at this point there is crosstalk between IL-1β and CBD signaling which results in phenotype reversion. Our 6D cell system allowed step-by-step analysis of the phenotype transition and better understanding of mechanisms by which CBD blocks and reverts the effects of inflammatory IL-1β in the EMT.

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IL-1β induces up-regulation of BIRC3, a gene involved in chemoresistance to doxorubicin in breast cancer cells

Cited by 61 publications

References 34 publications

FRAS1-related extracellular matrix protein 2 drives the progression and poor prognosis of IL-1β-associated esophageal squamous cell carcinoma

FRAS1-related extracellular matrix protein 2 drives the progression and poor prognosis of IL-1β-associated esophageal squamous cell carcinoma

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

CBD Reverts the Mesenchymal Invasive Phenotype of Breast Cancer Cells Induced by the Inflammatory Cytokine IL-1β

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