NFKB1 and Associated Diseases
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Overview of NFKB1
Nuclear factor kappa B subunit 1 (NFKB1, also known as nuclear factor NF-kappa-B p105 subunit) is a protein encoded by the NFKB1 gene in humans. NFKB1 is a 105 kD protein and produces a 50 kD protein after the cotranslational processing by the 26S proteasome. The 105 kD isoform functions as Rel protein-specific transcription inhibitor while the 50 kD protein is a subunit of the NF-κB protein complex with DNA binding ability. NF-κB, as a transcription factor, can be activated by various stimuli such as cytokines and ultraviolet irradiation, then the activated NF-κB translocates into the nucleus and initiates the gene expression involved in a wide range of biological processes.
NFKB1 in Disease
Inappropriate activation of NF-κB is related to inflammatory diseases while persistent inhibition of NF-κB leads to inappropriate immune cell development. Mutants in NFKB1 are associated with diseases such as atherosclerosis, cancer like ovarian cancer, and aging-associated diseases.
- Atherosclerosis
The circ_0005699/miR-450b-5P/NFKB1 axis is linked to the progress of atherosclerosis (AS). AS is regarded as the main pathological cause of cardiovascular diseases and vascular endothelial cell dysfunction is one of the critical events resulting in this pathology. In ApoE-deficient mice, as an AS model, upregulated expression of circ_0005699 and inflammatory cytokines can be observed. RNA pull-down assay indicates that circ_0005699 can bind miR-450b-5p and decrease its expression. NFKB1 is the target gene of miR-450b-5p. Knockdown of circ_0005699 leads to increased survival of the vascular endothelial cells and decreased expression of NFKB1 and inflammatory cytokines, which means enhanced repair of endothelial cell injury. Overexpression of NFKB1 can reverse the improved survival. Taken together, the regulation of circ_0005699/miR-450b-5P/NFKB1 axis may have beneficial effects in AS patients.
- Ovarian cancer
MAFG-AS1/NFKB1/IGF1 axis stimulates ovarian cancer (OC) malignant progression. OC is regarded as the 7th most common cancer affecting women across the globe. High expression of MAFG-AS1 can be found in OC tissues and associated cells. MAFG-AS1 can upregulate NFKB1 expression by binding to miR-339-5p, and elevated NFKB1 can induce IGF1 expression. The silence of NFKB1 will reverse the accelerated epithelial-mesenchymal transition, invasion, and migration of OC induced by MAFGAS1 overexpression. Besides, this phenomenon can be recapitulated in xenograft mice. In summary, MAFG-AS1/NFKB1/IGF1 axis sheds new light on the potential therapeutic target against OC.
Fig.1 Knockdown of NFKB1 can decrease the invasion ability in the OC cell line. (Bai, 2022)
To assist our clients in the field of gene therapy, Creative Biolabs has highly qualified teams of professionals on staff. In response to your inquiries about gene therapy, we offer thorough, disease-specific answers. Please feel free to contact us for more details about your NFKB1 project.
References
- Chen, T.; et al. Knockdown of hsa_circ_0005699 attenuates inflammation and apoptosis induced by ox-LDL in human umbilical vein endothelial cells through regulation of the miR-450b-5p/NFKB1 axis. Mol Med Rep. 2022, 26: 290.
- Bai, Y.; et al. LncRNA MAFG-AS1 promotes the malignant phenotype of ovarian cancer by upregulating NFKB1-dependent IGF1. Cancer Gene Ther. 2022, 29: 277–291.
