Mechanistic studies revealed that compound 3 modulated NF-kB expression and its downstream oncogenic proteins involved in cancer cell proliferation and invasion.
The sesquiterpene-coumarin ether samarcandone provided a suitable framework to replace the apocarotenoid A-C ring system of strigol (<b>1</b>), replicating, after linking to a butenolide moiety, the activity of the natural phytohormone on Nrf2 and also showing potent NF-kB inhibitory activity, overall modulating two critical pathways of inflammation and cancer.
American Indians (N = 636) were recruited from two different tribal populations (NP and SW) as part of a study conducted as part of the Collaborative to Improve Native Cancer Outcomes P50 project.
Our findings point to p50 involvement in colorectal cancer development, through its engagement in the protumor activation of macrophages, and identify a candidate for prognostic and target therapeutic intervention.<i>Cancer </i>.
A significant association was also observed between NFKB1 and CD14 variants and the evolution of the lesions; interestingly, this association was with both progression and regression in the same direction, which could reflect the dual role of inflammation in cancer.
Results showed that the expression of NF-κB1 in human glioma tissues and glioma cell lines, SHG44 and U87, was significantly higher compared to noncancerous brain tissues and that the expression increased with increasing degrees of tumor malignancy.
As a key mediator of inflammation-induced cancer, miR-15b-5p enhances these therapeutic effects are mainly attributed to targeting of the NF-κB signaling pathway through negative regulation of NF-κB1 and one of its kinase complexes IKK-α. miR-15b-5p mediates NF-ĸB regulation by targeting the anti-apoptosis protein XIAP in vitro.
The results showed that NFKB1 and NFKBIA single-nucleotide polymorphisms and gastric cancer are related and that the combined effects of polymorphisms in two genes and the NFKBIA gene monomer increased the risk of gastric cancer, and it was found that in different types of gastric cancer (the cardia and non-cardia cancer), susceptible polymorphism sites and combined effects are different.
The overexpression of CD44 in cancer cells reroutes number of oncogenic pathways including the central Pi3K/Akt/NF-kB pathway leading to cancer progression and malignancy.
American Indians (N=636) were recruited from two different tribal populations (NP in South Dakota, SW in Arizona) as part of a study carried out as part of the Collaborative to Improve Native Cancer Outcomes P50 Project.
The NFKB1 -94ins/delATTG polymorphism was associated with a decreased risk of overall cancer in the homozygote model (DD vs. II): OR = 0.75, 95% CI = 0.64-0.87); heterozygote model (ID vs. II): OR = 0.91, 95% CI = 0.83-0.99; recessive model (DD vs. ID/II): OR = 0.81, 95% CI = 0.71-0.91; dominant model (ID/DD vs. II): OR = 0.86, 95% CI = 0.78-0.95; and allele contrast model (D vs.I): OR = 0.88, 95% CI = 0.81-0.95).
Pancreatic ductal adenocarcinoma (PDAC) is a deadly cancer in which NF-κB pathways promote biological aggressiveness.In this issue of the JCI, Lesina et al. investigated the role of RelA, the p65 partner of p50 that together form the most common NF-κB complex, in the early stages of pancreatic malignant transformation and in established PDAC.
A functional -94 insertion/deletion ATTG polymorphism (rs28362491) in the promoter of the NFKB1 gene was reported to affect NF-KB1 expression and confer susceptibility to different types of cancer.
The subgroup analysis for ethnicity found that the NFKB1 -94ins/del ATTG promoter polymorphism was significantly associated with an increased susceptibility to cancer in Asians and with a decreased susceptibility in Caucasians.
Therefore, while the majority of research in this field has focused on the upstream signalling pathways leading to NF-κB activation or the function of other NF-κB subunits, such as RelA (p65), these data demonstrate a critical role for NFKB1, potentially revealing new strategies for targeting this pathway in inflammatory diseases and cancer.
An in-depth analysis indicated that NF-kB is activated and signals survival pathway contained the most cancer genes (number = 7), in which there was a hub cancer gene UBC.