AP-1 Is a Key Regulator of Proinflammatory Cytokine TNFα-mediated Triple-negative Breast Cancer Progression

Qiao, Yichun; He, Huan; Jonsson, Philip; Sinha, Indranil; Zhao, Chunyan; Dahlman-Wright, Karin

doi:10.1074/jbc.m115.702571

Cited by 96 publications

(62 citation statements)

References 42 publications

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“…Qiao et al demonstrated that TNFα induces apoptosis in BT549 cells, activating c-Jun which, in turn, downregulates anti-apoptotic genes, and upregulates pro-apoptotic cascades. In the same study, they showed that TNFα can also have a pro-malignant effect, stimulating c-Jun and inducing cell invasion (126). Other groups have proved that treatment with exogenous TNFα cannot trigger apoptosis in MDA-MB-468 (127) and MDA-MB-231 cell lines (130).…”

Section: Tnbc Subtypementioning

confidence: 94%

“…Regarding TNFα, there have been paradoxical results of its implication in TNBC proliferation and survival. It has been stated that TNFα can induce apoptosis (126) and promote tumor growth in TNBC, depending on the specific cell line and the cellular context in which it is found (127)(128)(129). Qiao et al demonstrated that TNFα induces apoptosis in BT549 cells, activating c-Jun which, in turn, downregulates anti-apoptotic genes, and upregulates pro-apoptotic cascades.…”

Section: Tnbc Subtypementioning

confidence: 99%

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Tumor Necrosis Factor α Blockade: An Opportunity to Tackle Breast Cancer

et al. 2020

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Breast cancer is the most frequently diagnosed cancer and the principal cause of mortality by malignancy in women and represents a main problem for public health worldwide. Tumor necrosis factor α (TNFα) is a pro-inflammatory cytokine whose expression is increased in a variety of cancers. In particular, in breast cancer it correlates with augmented tumor cell proliferation, higher malignancy grade, increased occurrence of metastasis and general poor prognosis for the patient. These characteristics highlight TNFα as an attractive therapeutic target, and consequently, the study of soluble and transmembrane TNFα effects and its receptors in breast cancer is an area of active research. In this review we summarize the recent findings on TNFα participation in luminal, HER2-positive and triple negative breast cancer progression and metastasis. Also, we describe TNFα role in immune response against tumors and in chemotherapy, hormone therapy, HER2-targeted therapy and anti-immune checkpoint therapy resistance in breast cancer. Furthermore, we discuss the use of TNFα blocking strategies as potential therapies and their clinical relevance for breast cancer. These TNFα blocking agents have long been used in the clinical setting to treat inflammatory and autoimmune diseases. TNFα blockade can be achieved by monoclonal antibodies (such as infliximab, adalimumab, etc.), fusion proteins (etanercept) and dominant negative proteins (INB03). Here we address the different effects of each compound and also analyze the use of potential biomarkers in the selection of patients who would benefit from a combination of TNFα blocking agents with HER2-targeted treatments to prevent or overcome therapy resistance in breast cancer.

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Section: Tnbc Subtypementioning

confidence: 94%

Section: Tnbc Subtypementioning

confidence: 99%

Tumor Necrosis Factor α Blockade: An Opportunity to Tackle Breast Cancer

et al. 2020

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“…In each case, key regulatory factors for each cell lineage recruit CRCs or HMCs to their target genes. Some TFs that are enumerated in this review, including OCT4, GATA1, GATA3, p53, and NF‐κB, are categorized as “pioneer” transcription factors (Iwafuchi‐Doi & Zaret, ; Mayran & Drouin, ; Qiao et al, ; Sammons, Zhu, Drake, & Berger, ). Pioneer factors play crucial roles in initiating cell programing and reprogramming, and they have the ability to recognize their target sequences in compacted or closed chromatin and then locally open the chromatin structure to provide accessibility to nonpioneer TFs (Iwafuchi‐Doi, ).…”

Section: Discussionmentioning

confidence: 99%

Enhancer function regulated by combinations of transcription factors and cofactors

et al. 2018

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Regulation of the expression of diverse genes is essential for making possible the complexity of higher organisms, and the temporal and spatial regulation of gene expression allows for the alteration of cell types and growth patterns. A critical component of this regulation is the DNA sequence-specific binding of transcription factors (TFs). However, most TFs do not independently participate in gene transcriptional regulation, because they lack an effector function. Instead, TFs are thought to work by recruiting cofactors, including Mediator complex (Mediator), chromatin-remodeling complexes (CRCs), and histone-modifying complexes (HMCs). Mediator associates with the majority of transcribed genes and acts as an integrator of multiple signals. On the other hand, CRCs and HMCs are selectively recruited by TFs. Although all the pairings between TFs and CRCs or HMCs are not fully known, there are a growing number of established TF-CRC and TF-HMC combinations. In this review, we focused on the most important of these pairings and discuss how they control gene expression.

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“…These additional cell types include components of the blood and lymph vasculature, tissue macrophages and lymphocytes, and various stromal fibroblasts and their derivatives. Both the infiltrating leukocytes and resident cancer‐associated fibroblasts (CAFs) are now well established as playing significant roles in modulating breast cancer cell growth and plasticity through direct interactions as well as through their secretion of growth factors, cytokines, and extracellular matrix components (Allinen et al, ; Aboussekhra, ; Place et al, ; Esquivel‐Velázquez et al, ; Qiao et al, ).…”

Section: Altered Transcriptional Regulation In Human Breast Cancersmentioning

confidence: 99%

Transcriptional regulation of normal human mammary cell heterogeneity and its perturbation in breast cancer

et al. 2019

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The mammary gland in adult women consists of biologically distinct cell types that differ in their surface phenotypes. Isolation and molecular characterization of these subpopulations of mammary cells have provided extensive insights into their different transcriptional programs and regulation. This information is now serving as a baseline for interpreting the heterogeneous features of human breast cancers. Examination of breast cancer mutational profiles further indicates that most have undergone a complex evolutionary process even before being detected. The consequent intra‐tumoral as well as inter‐tumoral heterogeneity of these cancers thus poses major challenges to deriving information from early and hence likely pervasive changes in potential therapeutic interest. Recently described reproducible and efficient methods for generating human breast cancers de novo in immunodeficient mice transplanted with genetically altered primary cells now offer a promising alternative to investigate initial stages of human breast cancer development. In this review, we summarize current knowledge about key transcriptional regulatory processes operative in these partially characterized subpopulations of normal human mammary cells and effects of disrupting these processes in experimentally produced human breast cancers.

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AP-1 Is a Key Regulator of Proinflammatory Cytokine TNFα-mediated Triple-negative Breast Cancer Progression

Cited by 96 publications

References 42 publications

Tumor Necrosis Factor α Blockade: An Opportunity to Tackle Breast Cancer

Tumor Necrosis Factor α Blockade: An Opportunity to Tackle Breast Cancer

Enhancer function regulated by combinations of transcription factors and cofactors

Transcriptional regulation of normal human mammary cell heterogeneity and its perturbation in breast cancer

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