LncNFYC-AS1 ameliorates Mycoplasma pneumoniae pneumonia via regulating miR-1323.

BACKGROUND

Mycoplasma 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.

METHODS

In 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.

RESULTS

NFYC-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.

CONCLUSION

NFYC-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.