Downregulation of miR-182-5p by NFIB promotes NAD+ salvage synthesis in colorectal cancer by targeting NAMPT

Bibliographic Details
Title: Downregulation of miR-182-5p by NFIB promotes NAD+ salvage synthesis in colorectal cancer by targeting NAMPT
Authors: Li Zhou, Hongtao Liu, Zhiji Chen, Siyuan Chen, Junyu Lu, Cao Liu, Siqi Liao, Song He, Shu Chen, Zhihang Zhou
Source: Communications Biology, Vol 6, Iss 1, Pp 1-12 (2023)
Publisher Information: Nature Portfolio, 2023.
Publication Year: 2023
Collection: LCC:Biology (General)
Subject Terms: Biology (General), QH301-705.5
More Details: Abstract Nuclear factor I B (NFIB) plays an important role in tumors. Our previous study found that NFIB can promote colorectal cancer (CRC) cell proliferation in acidic environments. However, its biological functions and the underlying mechanism in CRC are incompletely understood. Nicotinamide adenine dinucleotide (NAD+) effectively affects cancer cell proliferation. Nevertheless, the regulatory mechanism of NAD+ synthesis in cancer remains to be elucidated. Here we show NFIB promotes CRC proliferation in vitro and growth in vivo, and down-regulation of NFIB can reduce the level of NAD+. In addition, supplementation of NAD+ precursor NMN can recapture cell proliferation in CRC cells with NFIB knockdown. Mechanistically, we identified that NFIB promotes CRC cell proliferation by inhibiting miRNA-182-5p targeting and binding to NAMPT, the NAD+ salvage synthetic rate-limiting enzyme. Our results delineate a combination of high expression of NFIB and NAMPT predicted a clinical poorest prognosis. This work provides potential therapeutic targets for CRC treatment.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 2399-3642
Relation: https://doaj.org/toc/2399-3642
DOI: 10.1038/s42003-023-05143-z
Access URL: https://doaj.org/article/554f682c93a44fc082f071049689beee
Accession Number: edsdoj.554f682c93a44fc082f071049689beee
Database: Directory of Open Access Journals
More Details
ISSN:23993642
DOI:10.1038/s42003-023-05143-z
Published in:Communications Biology
Language:English