NF-κB Signaling in Tumor Pathways Focusing on Breast and Ovarian Cancer

Devanaboyina, Monika; Kaur, J.; Whiteley, Emma; Lin, Leslie; Einloth, Katelyn; Morand, Susan; Stanbery, Laura; Hamouda, Danae; Nemunaitis, John

doi:10.3389/or.2022.10568

Cited by 20 publications

(15 citation statements)

References 113 publications

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“…In a recent finding, Monica et al reported the involvement of the NF-κB pathway towards resistance to endocrine and chemotherapies in breast cancer [108]. Furthermore, BRCA1 signalling, which is one of the prominent pathways activated in various cancer types including breast cancer and ovarian cancer, additionally possesses the capability to induce the NF-κB pathway [109].…”

Section: Nf-κb: One Of the Key Factors Linking Inflammation In Cancermentioning

confidence: 99%

Transcriptional Regulation during Aberrant Activation of NF-κB Signalling in Cancer

Deka

2023

Cells

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The NF-κB signalling pathway is a major signalling cascade involved in the regulation of inflammation and innate immunity. It is also increasingly recognised as a crucial player in many steps of cancer initiation and progression. The five members of the NF-κB family of transcription factors are activated through two major signalling pathways, the canonical and non-canonical pathways. The canonical NF-κB pathway is prevalently activated in various human malignancies as well as inflammation-related disease conditions. Meanwhile, the significance of non-canonical NF-κB pathway in disease pathogenesis is also increasingly recognized in recent studies. In this review, we discuss the double-edged role of the NF-κB pathway in inflammation and cancer, which depends on the severity and extent of the inflammatory response. We also discuss the intrinsic factors, including selected driver mutations, and extrinsic factors, such as tumour microenvironment and epigenetic modifiers, driving aberrant activation of NF-κB in multiple cancer types. We further provide insights into the importance of the interaction of NF-κB pathway components with various macromolecules to its role in transcriptional regulation in cancer. Finally, we provide a perspective on the potential role of aberrant NF-κB activation in altering the chromatin landscape to support oncogenic development.

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Section: Nf-κb: One Of the Key Factors Linking Inflammation In Cancermentioning

confidence: 99%

Transcriptional Regulation during Aberrant Activation of NF-κB Signalling in Cancer

Deka

2023

Cells

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“…Dysregulated NF‐κB signaling has been implicated in the development of many human cancers. IκB proteins control NF‐κB activity (Devanaboyina et al, 2022). When inactive, NF‐κB complexes reside in the cytoplasm and bind to IκB.…”

Section: Targeting Bcl‐2 Family Proteins At the Transcriptional And P...mentioning

confidence: 99%

Comprehensive review of Bcl‐2 family proteins in cancer apoptosis: Therapeutic strategies and promising updates of natural bioactive compounds and small molecules

Iksen,

Witayateeraporn,

Hardianti

et al. 2024

Phytotherapy Research

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Cancer has a considerably higher fatality rate than other diseases globally and is one of the most lethal and profoundly disruptive ailments. The increasing incidence of cancer among humans is one of the greatest challenges in the field of healthcare. A significant factor in the initiation and progression of tumorigenesis is the dysregulation of physiological processes governing cell death, which results in the survival of cancerous cells. B‐cell lymphoma 2 (Bcl‐2) family members play important roles in several cancer‐related processes. Drug research and development have identified various promising natural compounds that demonstrate potent anticancer effects by specifically targeting Bcl‐2 family proteins and their associated signaling pathways. This comprehensive review highlights the substantial roles of Bcl‐2 family proteins in regulating apoptosis, including the intricate signaling pathways governing the activity of these proteins, the impact of reactive oxygen species, and the crucial involvement of proteasome degradation and the stress response. Furthermore, this review discusses advances in the exploration and potential therapeutic applications of natural compounds and small molecules targeting Bcl‐2 family proteins and thus provides substantial scientific information and therapeutic strategies for cancer management.

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“…In response to ionizing radiation, HER2 overexpression increases the activity of the PI3K/Akt pathway, which activates NF-κB and up-regulates pro-survival genes including manganese superoxide dismutase (MnSOD), cyclin B1, and HER2 [ 67 ]. Moreover, HER2 can mediate the stimulation of the canonical NF-κB, then subsequently mediates the formation and maintenance of the EMT [ 68 ]. The initiation of EMT involves the induction of numerous transcription regulators, including the Smad-interacting proteins ZEP-1/ZFHX1A, ZEB-2/ZFHX1B, SLUG, SIP1, and TWIST1 by the RelA molecule [ 68 ].…”

Section: Nf-κb In Bcmentioning

confidence: 99%

“…Moreover, HER2 can mediate the stimulation of the canonical NF-κB, then subsequently mediates the formation and maintenance of the EMT [ 68 ]. The initiation of EMT involves the induction of numerous transcription regulators, including the Smad-interacting proteins ZEP-1/ZFHX1A, ZEB-2/ZFHX1B, SLUG, SIP1, and TWIST1 by the RelA molecule [ 68 ]. Likewise, estrogen increases the transcription of IKK-α , ERs , and steroid coactivator 3 (SRC3) by binding to a particular area on the cyclin D1 promoter.…”

Section: Nf-κb In Bcmentioning

confidence: 99%

“…Cytokines of various types (TNF-α, interferon gamma (IFN-γ), and IL-17) and their interaction with NF-κB are reported to overexpress PD-L1 [ 78 ]. Additionally, PD-L1 transcription is induced via a process requiring MUC-1-mediated NF-κB activation [ 68 ]. Moreover, EGFR was also reported to induce PD-L1 transcription through its interaction with NF-κB.…”

Section: Nf-κb In Bcmentioning

confidence: 99%

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The NF-κB Transcriptional Network Is a High-Dose Vitamin C-Targetable Vulnerability in Breast Cancer

et al. 2023

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Breast cancer (BC) is the most common cancer type among women with a distinct clinical presentation, but the survival rate remains moderate despite advances in multimodal therapy. Consequently, a deeper understanding of the molecular etiology is required for the development of more effective treatments for BC. The relationship between inflammation and tumorigenesis is well established, and the activation of the pro-inflammatory transcription factor nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) is frequently identified in BC. Constitutive NF-κB activation is linked to cell survival, metastasis, proliferation, and hormonal, chemo-, and radiotherapy resistance. Moreover, the crosstalk between NF-κB and other transcription factors is well documented. It is reported that vitamin C plays a key role in preventing and treating a number of pathological conditions, including cancer, when administered at remarkably high doses. Indeed, vitamin C can regulate the activation of NF-κB by inhibiting specific NF-κB-dependent genes and multiple stimuli. In this review, we examine the various NF-κB impacts on BC development. We also provide some insight into how the NF-κB network may be targeted as a potential vulnerability by using natural pro-oxidant therapies such as vitamin C.

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NF-κB Signaling in Tumor Pathways Focusing on Breast and Ovarian Cancer

Cited by 20 publications

References 113 publications

Transcriptional Regulation during Aberrant Activation of NF-κB Signalling in Cancer

Transcriptional Regulation during Aberrant Activation of NF-κB Signalling in Cancer

Comprehensive review of Bcl‐2 family proteins in cancer apoptosis: Therapeutic strategies and promising updates of natural bioactive compounds and small molecules

The NF-κB Transcriptional Network Is a High-Dose Vitamin C-Targetable Vulnerability in Breast Cancer

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