RESUMEN
The MASS cohort comprises 2000 ICU patients with severe pneumonia, covering community-acquired pneumonia, hospital-acquired pneumonia, and ventilator-associated pneumonia, sourced from 19 hospitals across 10 cities in three provinces. A wide array of samples including bronchoalveolar lavage fluid, sputum, feces, and whole blood are longitudinally collected throughout patients' ICU stays. The cohort study seeks to uncover the dynamics of lung and gut microbiomes and their associations with severe pneumonia and host susceptibility, integrating deep metagenomics and transcriptomics with detailed clinical data.
RESUMEN
Studies demonstrate that long non-coding RNAs (lncRNAs) play vital roles in cancer progression. However, the expression pattern and molecular mechanisms of lncRNA FAM83A-AS1 in lung cancer remain largely unclear. Here, we analyzed FAM83A-AS1 expression in lung cancer tissues from three RNA-sequencing (RNA-Seq) datasets and validated these results using quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) in an independent set of lung adenocarcinoma. Cell proliferation, migration, invasion, and autophagy were analyzed after knockdown FAM83A-AS1 with siRNAs. The underlying molecular mechanisms of FAM83A-AS1 were performed by Western blot, qRT-PCR, and RNA-seq analysis. We found that FAM83A-AS1 was up-regulated in lung cancer and elevated expression was associated with poor patient survival. These results were confirmed using RT-PCR in an independent set of lung cancer. Functional study indicated that FAM83A-AS1 knockdown reduced cell proliferation, migration, invasion, and colony formation in cancer cells. FAM83A-AS1 silencing induced autophagy and cell cycle arrest at G2. Mechanistically, serval oncogenic proteins such as EGFR, MET, PI3K, and K-RAS were decreased upon FAM83A-AS1 silencing, while phosphor AMPKα and ULK1 were increased. Based on the above results, we believe that FAM83A-AS1 may have potential as a diagnosis/prognosis marker and its oncogenic role and autophagy regulation may be through MET-AMPKα signaling, which could lead to potential targeting for lung cancer therapy.