The NF-?B family of dimeric transcription factors mediates critical biological functions in inflammation, innate immunity, cell proliferation and survival. In contrast, deregulation of NF-?B pathway components has been causally linked to the development of pathological processes including cancers, inflammatory and metabolic disorders. The complex roles of NF-?B in a multitude of cellular processes and diseases could be attributed to the hundreds of target genes whose expression are regulated by NF-?B factors involving transcriptional or epigenetic mechanisms. While previous investigations were mostly focused on the regulation of classical NF-?B pathway, there is increasing evidence for noncanonical NF-?B functions in inflammation and cancer. The microbiome also plays significant roles in regulating NF-?B signaling and abnormal perturbations in gut microbiota are associated with the incidence of diseases such as inflammatory bowel disease, Parkinson’s disease, type 2 diabetes mellitus and cancer, adding a new dimension to the biology of modern diseases. Although the aetiologies of these complex diseases are multifactorial, the involvement of several inflammatory loops are quite evident. NF-?B, being a key regulator in the crosstalk between multiple inflammatory pathways, serves as a matchmaker between inflammation and these modern diseases.
This Research Topic seeks to cover outstanding research illustrating recent developments in the regulatory roles of NF-?B factors in inflammation and cancer, as well as novel investigations which explore the tripartite link between microbiota, NF-?B and modern diseases.
Specific areas to be covered in this Research Topic may include the following:
1. NF-?B mediated transcriptional or epigenetic mechanisms in inflammation and cancer
2. Transcriptional specificity of NF-?B factors in inflammation and cancer
3. Role of NF-?B signaling in tumor-promoting inflammation
4. Regulation of NF-?B signaling by gut microbiota in health and disease
5. NF-?B signaling in stem cells and development, particularly cancer stem cells
6. Role of NF-?B associated long non-coding RNAs (lncRNAs) in inflammation and cancer progression
7. Role of noncanonical NF-?B signaling in inflammation and cancer
A full list of accepted article types, including descriptions, can be found at this
link
![GM114 attenuates DSS-induced acute colitis. (A) Gm114+/+ and Gm114−/− mice were treated with 5% (w/v) DSS in drinking water for 5 days, followed by 9 days of normal drinking water. Body weight changes were recorded daily until the mice had mostly died (day 8). Data represent the weight change relative to each individual starting weight. (B,C) Gm114+/+ and Gm114−/− mice were treated with 2.5% (w/v) DSS in drinking water for 7 days, followed by 7 days of normal drinking water. Mice were sacrificed on day 14 to measure the colon length. (D) Mice were treated as described in (A). Composite DAI scores were determined by assessing weight loss, stool consistency, and the presence of blood in stool and/or the rectum at day 5 after DSS treatment. (E,F) Mice were treated as described in (B). Representative H&E-stained sections of colons from mock- and DSS-treated Gm114+/+ and Gm114−/− mice (14 days). Scale bar represents 50 μm (E). Histological scores of inflammation-associated changes in the colon were assessed as shown in (F). (G) Mice were treated as described in (B). qPCR was conducted to measure the mRNA levels of Il6, Il-1β and Tnfα in colons from Gm114+/+ and Gm114−/− mice at day 14 after 2.5% DSS administration. (H) Mice were treated as described in (B). Colons from Gm114+/+ and Gm114−/− mice at day 14 after 2.5% DSS administration were harvested for immunoblotting (left panel), and densitometric analysis was shown in right panel. (I) Mice were treated as described in (B). Sera were collected at days 7 and 14 after DSS administration to measure IL-6 production by an ELISA. (J) Mice were treated as described in (A). Survival rates of Gm114+/+ and Gm114−/− mice were monitored daily. Data shown in (A,C,D,F,G,I,J) are from one representative experiment of three independent experiments [mean ± SD, n = 3 in (G)]. *p < 0.05; **p < 0.01; ***p < 0.001; two-tailed Student’s t-test. The log-rank (Mantel–Cox) test was used in Data (J).](https://www.frontiersin.org/_rtmag/_next/image?url=https%3A%2F%2Fwww.frontiersin.org%2Ffiles%2FArticles%2F877039%2Ffcell-10-877039-HTML%2Fimage_m%2Ffcell-10-877039-g007.jpg&w=3840&q=75)
