ArticleCommunications biology2023
Downregulation of miR-182-5p by NFIB promotes NAD+ salvage synthesis in colorectal cancer by targeting NAMPT.
Article in Communications biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 11 citations in OpenAlex.
- Aging and cancer: current understandings and future perspectives.Signal transduction and targeted therapy · 2026Review
- Why is the tumor microenvironment disordered by NADH/NADRedox biology · 2026Review
- CDCP1/mitochondrial Src axis increases electron transport chain function to promote metastasis in triple-negative breast cancer.British journal of cancer · 2025Article
- The multifaceted role of microRNAs in colorectal cancer: pathogenesis and therapeutic implications.Non-coding RNA research · 2025Review
- The Role of MCM7 and Its Hosted miR-106b-25 Cluster in Renal Cancer Progression.International journal of molecular sciences · 2025Article
- Single-cell sequencing reveals the role ofiMeta · 2025Article
- NADAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- MicroRNAs in the Diagnosis of Digestive Diseases: A Comprehensive Review.Journal of clinical medicine · 2025Review
- Identification of fibrosis-associated biomarkers in heart failure and human cancers.Journal of translational medicine · 2024Article
- PCAT19: the role in cancer pathogenesis and beyond.Frontiers in cell and developmental biology · 2024Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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