ArticleAnnals of translational medicine2021
LncRNA NFYC-AS1 promotes the development of lung adenocarcinomas through autophagy, apoptosis, and MET/c-Myc oncogenic proteins.
Article in Annals of translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- LncNFYC-AS1 ameliorates Mycoplasma pneumoniae pneumonia via regulating miR-1323.BMC pulmonary medicine · 2025Article
- Integrating datasets to dissectData in brief · 2025Article
- Construction and validation of a prognostic model of lncRNAs associated with RNA methylation in lung adenocarcinoma.Translational cancer research · 2025Article
- The potential of targeting autophagy-related non-coding RNAs in the treatment of lung cancer.Frontiers in pharmacology · 2025Review
- Erratum to lncRNA NFYC-AS1 promotes the development of lung adenocarcinomas through autophagy, apoptosis, and MET/c-Myc oncogenic proteins.Annals of translational medicine · 2024Article
- [High expression of LINC00467 promotes proliferation and metastasis of lung adenocarcinoma cells by suppressing autophagyNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- The pancancer overexpressed NFYC Antisense 1 controls cell cycle mitotic progression through in cis and in trans modes of action.Cell death & disease · 2024Article
- Systematic integration of m6A regulators and autophagy-related genes in combination with long non-coding RNAs predicts survival in glioblastoma multiforme.Scientific reports · 2023Article
- LncRNA TEX41 regulates autophagy by increasing Runx2 expression in lung adenocarcinoma bone metastasis.American journal of translational research · 2023Article
- Review
- Identification of an autophagy-related 12-lncRNA signature and evaluation of NFYC-AS1 as a pro-cancer factor in lung adenocarcinoma.Frontiers in genetics · 2022Article
- Electroacupuncture induces weight loss by regulating tuberous sclerosis complex 1-mammalian target of rapamycin methylation and hypothalamic autophagy in high-fat diet-induced obese rats.Frontiers in pharmacology · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNuclear transcription factor Y subunit C antisense RNA 1 (NFYC-AS1) was revealed to be a potential prognostic biomarker in lung adenocarcinoma (LAUD) by analyzing The Cancer Genome Atlas (TCGA) database. However, the function of NFYC-AS1 has not been verified in cancers, including LAUD. We plan to verify the function of NFYC-AS1 in LAUD through this study.
methodsWe determined NFYC-AS1 expression in 4 LAUD cell lines, and 1 normal lung cell line (HBE) by quantitative real-time reverse transcription PCR (qRT-PCR). small interfering RNA (siRNA) was employed to specifically knockdown NFYC-AS1 in H1299 and PC9 cell lines. Cell growth and invasion activity of LAUD cells was assessed by WST-1, colony formation and transwell assay, respectively. The effect of NFYC-AS1 expression on cell apoptosis was then assessed by flow cytometry assay. Furthermore, the expression of downstream proteins of NFYC-AS1 was investigated by Western blot.
resultsThe proliferation, migration, and invasion of cells were inhibited and apoptosis was increased after NFYC-AS1 knockdown in LAUD cells. The cells transfected with NFYC-AS1 siRNA had a higher rate of apoptosis compared with that in control cells. The apoptosis-related proteins p53 and PARP were upregulated. These suggested NFYC-AS1 could inhibit the apoptosis of LAUD cells. In terms of the expression of major autophagy proteins, p62 was downregulated while Beclin 1 was upregulated after NFYC-AS1 knockdown, which suggested that autophagy was activated. The expression of oncogenic proteins MET and c-Myc was downregulated.
conclusionsIn summary, the above results suggest that NFYC-AS1 may promote the proliferation of LAUD through autophagy and apoptosis.
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