NF-κB-Related Genetic Diseases

Courtois, G.; Pescatore, Alessandra; Gautheron, Jérémie; Fusco, Francesca R.; Ursini, Matilde Valeria; Senegas, Anna

doi:10.1007/978-3-319-25850-8

Cited by 8 publications

(9 citation statements)

References 44 publications

(99 reference statements)

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“…NF-κB is another transcription factor that is important for EMT via the regulation of SNAIL and Twist expression in breast, renal and colon cancer (23)(24)(25)41). Several reports have associated NF-κB with certain pathologies such as inflammation, cancer and chemotherapy resistance (20,23). The elevated expression of NF-κB p65 has been observed in ovarian and breast cancer, and has been associated with the clinical stage and the histological subtype (42,43).…”

Section: Discussionmentioning

confidence: 99%

“…NF-κB is activated by a wide variety of stimuli that include growth factors, cytokines, infectious agents and chemotherapy drugs, among others. Once activated, NF-κB is involved in the regulation of biological processes, such as proliferation, differentiation and apoptosis, and some pathologies, such as inflammation, cancer and chemotherapy resistance (20). The epithelial-mesenchymal transition (EMT) is a biological process in which a polarized epithelial cell normally interacts with the basement membrane via its basal surface, and undergoes a series of morphological and biochemical changes that allow it to adopt a mesenchymal phenotype (21,22).…”

Section: Introductionmentioning

confidence: 99%

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Paclitaxel resistance is mediated by NF‑κB on mesenchymal primary breast cancer cells

et al. 2021

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Paclitaxel has been used widely to treat breast cancer and other types of cancer. However, resistance is a major cause of failure for treatment and results in cancer progression. The present study investigated the association between paclitaxel resistance and the mesenchymal phenotype, using a model of primary breast cancer cells and employing four different cultures, two with an epithelial phenotype (MBCDF and MBCD17) and two with a mesenchymal phenotype (MBCDF-D5 and MBCD3). Epithelial-mesenchymal markers were evaluated by western blotting; MBCDF and MBCD17 cells expressed E-cadherin, SNAIL, Slug, and Twist, low levels of N-cadherin, but not vimentin. MBCDF-D5 and MBCD3 cells expressed N-cadherin, vimentin, and higher levels of SNAIL, and low levels of E-cadherin, Slug, and Twist. Cell viability was evaluated using a crystal violet assay after paclitaxel treatment; primary breast cancer cells with mesenchymal phenotype were resistant to paclitaxel compared with the epithelial primary breast cancer cells. Furthermore, using western blotting, it was revealed that mesenchymal cells had elevated levels of nuclear factor-κΒ (NF-κB) p65 and IκB kinase (IKK). Additionally, it was demonstrated that paclitaxel-induced degradation of the inhibitor of NF-κB, activation of NF-κB in a dose-dependent manner, and Bcl-2 and Bcl-xL upregulation. Finally, employing western blotting and crystal violet assays, the effects of the proteasome inhibitor ALLN were assessed. ALLN inhibited paclitaxel-induced NF-κB activation and restored the sensitivity to paclitaxel. Together, these data suggest that targeting the NF-κB/IKK axis might be a promising strategy to overcome paclitaxel resistance.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Paclitaxel resistance is mediated by NF‑κB on mesenchymal primary breast cancer cells

et al. 2021

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“…Knockout mice for the RHD proteins show predominantly immunological defects (Gerondakis et al, 2006). Also, a cornucopia of human genetic disorders affecting NF-κB show prominent immune pathology (Courtois et al, 2016). Correspondingly, CP inducers, mainly p50:RelA dimers, include all sorts of pro-inflammatory cytokines such as tumor necrosis factor (TNF) and interleukin-1 (IL-1), conventional humoral and cellular antigens, pathogen-associated molecular patterns (PAMPs) including many bacterial and viral products, cellbound and soluble immune mediators, and effector molecules.…”

Section: Biochemistrymentioning

confidence: 99%

30 Years of NF-κB: A Blossoming of Relevance to Human Pathobiology

Zhang

Lenardo

Baltimore

2017

Cell

1,546

1,374

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NF-κB was discovered thirty years ago as a rapidly inducible transcription factor. Since that time it has been found to have a broad role in gene induction in diverse cellular responses, particularly throughout the immune system. Here we summarize elaborate regulatory pathways involving this transcription factor and use recent discoveries in human genetic diseases to place specific proteins within their relevant medical and biological contexts.

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“…The inhibition of this pathway through I κ B α in transgenic mice results in a phenotype similar to HED . In addition to EDA, EDAR, and EDARADD, other molecules of EDA pathway have been implicated with HED …”

Section: Molecular Bases Of Ectodermal Dysplasiasmentioning

confidence: 99%

“…The implication of NF κ B signaling in ectodermal appendages is quite interesting because this factor is well known for its major role during inflammation and immunity, acting downstream of the activation of TNF immune receptors, contrasting with its role when it is activated by EDA pathway, where it does not seem to induce inflammation. However, recent data suggests the participation of the EDA pathway in the induction of chemokines transcription …”

Section: Molecular Bases Of Ectodermal Dysplasiasmentioning

confidence: 99%

Hypohidrotic ectodermal dysplasia: clinical and molecular review

et al. 2018

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Hypohidrotic Ectodermal Dysplasia (HED) is a genetic human disorder which affects structures of ectodermal origin. Although there are autosomal recessive and dominant forms, X-linked (XL) is the most frequent form of the disease. This XL-HED phenotype is associated with mutations in the gene encoding the transmembrane protein ectodysplasin-1 (EDA1), a member of the TNFα-related signaling pathway. The proteins from this pathway are involved in signal transduction from ectoderm to mesenchyme leading to the development of ectoderm-derived structures in the fetus such as hair, teeth, skin, nails, and eccrine sweat glands. The aim of this review was to update the main clinical characteristics of HED regarding to recent molecular advances in the comprehension of all the possible genes involved in this group of disorders since it is known that Eda-A1-Edar signaling has multiple roles in ectodermal organ development, regulating their initiation, morphogenesis, and differentiation steps. The knowledge of the biological mechanisms that generate HED is needed for both a better detection of possible cases and for the design of efficient prevention and treatment approaches.

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NF-κB-Related Genetic Diseases

Cited by 8 publications

References 44 publications

Paclitaxel resistance is mediated by NF‑κB on mesenchymal primary breast cancer cells

Paclitaxel resistance is mediated by NF‑κB on mesenchymal primary breast cancer cells

30 Years of NF-κB: A Blossoming of Relevance to Human Pathobiology

Hypohidrotic ectodermal dysplasia: clinical and molecular review

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