JunB: a paradigm for Jun family in immune response and cancer

Ren, Fu-jia; Cai, Xiao-yu; Yao, Yao; Fang, Guo-ying

doi:10.3389/fcimb.2023.1222265

Cited by 18 publications

(1 citation statement)

References 117 publications

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“…JUNB, as a component of activator protein-1 (AP-1), inhibits the cell cycle and induces senescence [78,79], thereby acting as a tumor suppressor in a variety of cancers. However, its overexpression was found to cause tumor progression in NSCLC [80]. EGOT encodes for a long noncoding RNA that has been reported to inhibit cell migration and proliferation in breast and renal cell carcinoma [81,82], but its role in NSCLC is unclear [83].…”

Section: Chronic Hypoxia Upregulates Nf-κb Target Genes Influencing C...mentioning

confidence: 99%

NF-κB in the Radiation Response of A549 Non-Small Cell Lung Cancer Cells to X-rays and Carbon Ions under Hypoxia

Nisar,

Sanchidrián González,

Labonté

et al. 2024

IJMS

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Cellular hypoxia, detectable in up to 80% of non-small cell lung carcinoma (NSCLC) tumors, is a known cause of radioresistance. High linear energy transfer (LET) particle radiation might be effective in the treatment of hypoxic solid tumors, including NSCLC. Cellular hypoxia can activate nuclear factor κB (NF-κB), which can modulate radioresistance by influencing cancer cell survival. The effect of high-LET radiation on NF-κB activation in hypoxic NSCLC cells is unclear. Therefore, we compared the effect of low (X-rays)- and high (12C)-LET radiation on NF-κB responsive genes’ upregulation, as well as its target cytokines’ synthesis in normoxic and hypoxic A549 NSCLC cells. The cells were incubated under normoxia (20% O2) or hypoxia (1% O2) for 48 h, followed by irradiation with 8 Gy X-rays or 12C ions, maintaining the oxygen conditions until fixation or lysis. Regulation of NF-κB responsive genes was evaluated by mRNA sequencing. Secretion of NF-κB target cytokines, IL-6 and IL-8, was quantified by ELISA. A greater fold change increase in expression of NF-κB target genes in A549 cells following exposure to 12C ions compared to X-rays was observed, regardless of oxygenation status. These genes regulate cell migration, cell cycle, and cell survival. A greater number of NF-κB target genes was activated under hypoxia, regardless of irradiation status. These genes regulate cell migration, survival, proliferation, and inflammation. X-ray exposure under hypoxia additionally upregulated NF-κB target genes modulating immunosurveillance and epithelial-mesenchymal transition (EMT). Increased IL-6 and IL-8 secretion under hypoxia confirmed NF-κB-mediated expression of pro-inflammatory genes. Therefore, radiotherapy, particularly with X-rays, may increase tumor invasiveness in surviving hypoxic A549 cells.

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Section: Chronic Hypoxia Upregulates Nf-κb Target Genes Influencing C...mentioning

confidence: 99%

NF-κB in the Radiation Response of A549 Non-Small Cell Lung Cancer Cells to X-rays and Carbon Ions under Hypoxia

Nisar,

Sanchidrián González,

Labonté

et al. 2024

IJMS

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JUNB O‐GlcNAcylation‐Mediated Promoter Accessibility of Metabolic Genes Modulates Distinct Epithelial Lineage in Pulmonary Fibrosis

Bammert,

Ansari,

Haag

et al. 2024

Advanced Science

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Idiopathic pulmonary fibrosis (IPF) is a lethal disease with substantial unmet medical needs. While aberrant epithelial remodeling is a key factor in IPF progression, the molecular mechanisms behind this process remain elusive. Harnessing a 3D patient‐derived organoid model and multi‐omics approach, the first inventory of the connection between metabolic alteration, chromatin accessibility, and transcriptional regulation in IPF aberrant epithelial remodeling is provided. This remodeling is characterized by an increase in chromatin accessibility, particularly at JUNB motif‐enriched promoter regions proximal to transcription start sites of metabolic and pro‐fibrotic genes. Mechanistically, JUNB undergoes O‐linked β‐N‐acetylglucosamine modification (O‐GlcNAcylation), a critical step in modulating pro‐fibrotic responses to chronic injury. This modification is pivotal in fostering the emergence of aberrant epithelial basal cells in the alveolar niche, a proposed driver of IPF pathology. Specific deletion of O‐GlcNAcylation sites on JUNB attenuates the metaplastic differentiation of basal cells, thereby aiding in the restoration of the alveolar lineage. Together, the findings reveal a novel link between metabolic dysregulation and cell fate regulation at the chromatin level in fibrosis, mediated by the O‐GlcNAc‐JUNB axis, suggesting avenues for the development of new therapeutic strategies in IPF.

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Dihydrocelastrol induces cell death and suppresses angiogenesis through BCR/AP-1/junb signalling in diffuse large B cell lymphoma

Lai,

Guo,

Tang

et al. 2024

Archives of Biochemistry and Biophysics

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JunB: a paradigm for Jun family in immune response and cancer

Cited by 18 publications

References 117 publications

NF-κB in the Radiation Response of A549 Non-Small Cell Lung Cancer Cells to X-rays and Carbon Ions under Hypoxia

NF-κB in the Radiation Response of A549 Non-Small Cell Lung Cancer Cells to X-rays and Carbon Ions under Hypoxia

JUNB O‐GlcNAcylation‐Mediated Promoter Accessibility of Metabolic Genes Modulates Distinct Epithelial Lineage in Pulmonary Fibrosis

Dihydrocelastrol induces cell death and suppresses angiogenesis through BCR/AP-1/junb signalling in diffuse large B cell lymphoma

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