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

Deka, Kamalakshi; Li, Yinghui

doi:10.3390/cells12050788

Cited by 31 publications

(12 citation statements)

References 248 publications

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“…The non-canonical NF-κB pathway has been documented to play critical roles in the progression of various malignancies and can be activated in response to a variety of ligands, including TWEAK 6 , 19 – 21 . To investigate the role of NF-κB/p52 in regulating the genomic occupancy of ETS1 in gliomas, we performed chromatin immunoprecipitation (ChIP) sequencing (ChIP-seq) using p52 and ETS1 antibodies in the glioma cell line, U-87 MG, with and without TWEAK treatment.…”

Section: Resultsmentioning

confidence: 99%

NF-κB/p52 augments ETS1 binding genome-wide to promote glioma progression

Sim

2023

Commun Biol

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Gliomas are highly invasive and chemoresistant cancers, making them challenging to treat. Chronic inflammation is a key driver of glioma progression as it promotes aberrant activation of inflammatory pathways such as NF-κB signalling, which drives cancer cell invasion and angiogenesis. NF-κB factors typically dimerise with its own family members, but emerging evidence of their promiscuous interactions with other oncogenic factors has been reported to promote transcription of new target genes and function. Here, we show that non-canonical NF-κB activation directly regulates p52 at the ETS1 promoter, activating its expression. This impacts the genomic and transcriptional landscape of ETS1 in a glioma-specific manner. We further show that enhanced non-canonical NF-κB signalling promotes the co-localisation of p52 and ETS1, resulting in transcriptional activation of non-κB and/or non-ETS glioma-promoting genes. We conclude that p52-induced ETS1 overexpression in glioma cells remodels the genome-wide regulatory network of p52 and ETS1 to transcriptionally drive cancer progression.

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Section: Resultsmentioning

confidence: 99%

NF-κB/p52 augments ETS1 binding genome-wide to promote glioma progression

Sim

2023

Commun Biol

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“…The continuous activation of NF-κB can initiate cyclinD1 transcription, promote the G1/G0 phase-to-S phase transition, and lead to abnormal cell proliferation and cancer. Thus, inhibiting NF-κB activation or blocking its downstream key proteins is considered an important target for developing new antitumor drugs ( Taniguchi and Karin, 2018 ; Deka and Li, 2023 ).…”

Section: Discussion On the Common Molecular Mechanism Of Sishen Pill ...mentioning

confidence: 99%

Sishen Pill and its active phytochemicals in treating inflammatory bowel disease and colon cancer: an overview

Zhang,

Cheng,

Jian

et al. 2024

Front. Pharmacol.

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The incidence of inflammatory bowel disease (IBD) and the associated risk of colon cancer are increasing globally. Traditional Chinese medicine (TCM) treatment has unique advantages. The Sishen Pill, a common Chinese patented drug used to treat abdominal pain and diarrhea, consists mainly of Psoraleae Fructus, Myristicae Semen, Euodiae Fructus, and Schisandra Chinensis. Modern research has confirmed that Sishen Pill and its active secondary metabolites, such as psoralen, myristicin, evodiamine, and schisandrin, can improve intestinal inflammation and exert antitumor pharmacological effects. Common mechanisms in treating IBD and colon cancer mainly include regulating inflammation-related signaling pathways such as nuclear factor-kappa B, mitogen-activated protein kinase, phosphatidylinositol 3-kinase, NOD-like receptor heat protein domain-related protein 3, and wingless-type MMTV integration site family; NF-E2-related factor 2 and hypoxia-inducible factor 1α to inhibit oxidative stress; mitochondrial autophagy and endoplasmic reticulum stress; intestinal immune cell differentiation and function through the Janus kinase/signal transducer and activator of transcription pathway; and improving the gut microbiota and intestinal barrier. Overall, existing evidence suggests the potential of the Sishen pill to improve IBD and suppress inflammation-to-cancer transformation. However, large-scale randomized controlled clinical studies and research on the safety of these clinical applications are urgently required.

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“… 41 Activation of the NF-κB pathway is observed in multiple cancers and plays a role in their occurrence and progression. 42 In pancreatic cancer, NF-κB has been implicated in processes such as proliferation, invasion, and metastasis. 13 , 14 Furthermore, a prior study has indicated that the regulation of NUAK2 depends on the activation of NF-κB.…”

Section: Discussionmentioning

confidence: 99%

The NF-κB/NUAK2 signaling axis regulates pancreatic cancer progression by targeting SMAD2/3

Wang,

Su,

Liu

et al. 2024

iScience

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

Cited by 31 publications

References 248 publications

NF-κB/p52 augments ETS1 binding genome-wide to promote glioma progression

NF-κB/p52 augments ETS1 binding genome-wide to promote glioma progression

Sishen Pill and its active phytochemicals in treating inflammatory bowel disease and colon cancer: an overview

The NF-κB/NUAK2 signaling axis regulates pancreatic cancer progression by targeting SMAD2/3

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