ArticleMolecular medicine reports2016
Transcription factor NF‑YA promotes a malignant phenotype by upregulating fatty acid synthase expression.
Article in Molecular medicine reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- NFYA-mediated promotion of castration-resistant prostate cancer progression through EGR4 regulation.Discover oncology · 2024Article
- Live cell dynamics of the NF-Y transcription factor.Scientific reports · 2021Article
- Transcription factor NFYA promotes G1/S cell cycle transition and cell proliferation by transactivating cyclin D1 and CDK4 in clear cell renal cell carcinoma.American journal of cancer research · 2020Article
- Anoikis resistant mediated by FASN promoted growth and metastasis of osteosarcoma.Cell death & disease · 2019Article
- Role of oxidative stress in Retinitis pigmentosa: new involved pathways by an RNA-Seq analysis.Cell cycle (Georgetown, Tex.) · 2019Article
- LINC01016 promotes the malignant phenotype of endometrial cancer cells by regulating the miR-302a-3p/miR-3130-3p/NFYA/SATB1 axis.Cell death & disease · 2018Article
- The animal nuclear factor Y: an enigmatic and important heterotrimeric transcription factor.American journal of cancer research · 2018Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies have revealed that increased expression of the alpha subunit of nuclear transcription factor Y (NF‑YA) is associated with the malignant phenotype of various tumors. However, whether elevated expression of NF‑YA promotes a malignant phenotype in osteosarcoma (OS), and the molecular mechanisms underlying this predicted effect is currently unknown. In the present study, small hairpin RNA (shRNA)‑mediated knockdown of endogenous NF‑YA significantly inhibited the migration and invasion capabilities of OS cells in vitro, whereas ectopic expression of NF‑YA increased the migration and invasion capabilities of these cells. In addition, the induction of upregulated NF‑YA expression on the malignant phenotype of OS cells was attenuated by silencing fatty acid synthase (FASN) expression. Furthermore, the expression level of FASN was increased by upregulating NF‑YA, while decreased FASN expression was observed following NF‑YA silencing in OS cells. The results of the present study suggest that NF‑YA may promote a malignant phenotype in OS cells, in part, by activating the FASN signaling pathway, which may represent a promising target for the management of OS.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.