ArticleBMC pulmonary medicine2025
LncNFYC-AS1 ameliorates Mycoplasma pneumoniae pneumonia via regulating miR-1323.
Article in BMC pulmonary medicine, 2025. 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 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Exosomal lncRNA DLEU2 aggravates inflammatory injury and apoptosis in pediatric viral pneumonia via the miR-330-5p.Hereditas · 2026Article
- Correction: LncNFYC-AS1 ameliorates Mycoplasma pneumoniae pneumonia via regulating miR- 1323.BMC pulmonary medicine · 2026Article
Corrections and comments
- Erratum issued
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMycoplasma pneumoniae pneumonia (MPP) is a common respiratory infection, yet its molecular mechanisms remain incompletely understood. Long non-coding RNAs (lncRNAs) play critical roles in various diseases, but their regulatory functions in MPP require further investigation. This study aimed to investigate the expression profile and clinical significance of NFYC-AS1 in MPP and analyze its interaction with miR-1323 in modulating cellular functions.
methodsIn vitro cell culture methods were used to establish MPP cell models, and A549 cells were transfected to introduce or inhibit lncRNAs and miRNAs. Real-time quantitative PCR was used to detect the expression levels of NFYC-AS1 and miR-1323. The direct binding relationship between NFYC-AS1 and miR-1323 was verified using a luciferase reporter gene assay. Elisa was used to quantify the levels of cytokines TNF-α, IL-1β, and IL-6. CCK-8 assay was employed to assess cell growth capacity. Transwell analysis was used to study cell migration. Cell apoptosis rates were detected by flow cytometry. Finally, statistical analysis methods were used to process and interpret the data.
resultsNFYC-AS1 was significantly upregulated in patients and significantly associated with MPP risk, showing a negative correlation with miR-1323. Mechanistically, NFYC-AS1 directly targeted and suppressed miR-1323. In MP-infected A549 cells, NFYC-AS1 knockdown reduced inflammatory cytokines (TNF-α/IL-1β/IL-6), enhanced proliferation/migration, and inhibited apoptosis-effects abolished by miR-1323 inhibition.
conclusionNFYC-AS1 is highly expressed in MPP and regulates inflammatory responses, cell proliferation, migration, and apoptosis by targeting miR-1323. The NFYC-AS1/miR-1323 axis may serve as a potential therapeutic target and show preliminary discriminatory value for MPP.
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