Chronic obstructive pulmonary disease (
COPD) is a global high-incidence chronic airway
inflammation disease. Its deterioration will lead to more serious lung lesions and even
lung cancer. Therefore, it is urgent to determine the pathogenesis of
COPD and find potential therapeutic targets. The purpose of this study is to reveal the molecular mechanism of
COPD disease development through in-depth analysis of
transcription factors and ncRNA-driven pathogenic modules of
COPD. We obtained the expression profile of
COPD-related
microRNAs from the NCBI-GEO database and analyzed the differences among groups to identify the
microRNAs significantly associated with
COPD. Then, their target genes are predicted and mapped to a
protein-
protein interaction (PPI) network. Finally, key
transcription factors and the ncRNA of the regulatory module were identified based on the hypergeometric test. The results showed that CUL1 was the most interactive gene in the highly interactive module, so it was recognized as a dysfunctional molecule of
COPD. Enrichment analysis also showed that it was much involved in the biological process of organelle fission, the highest number of regulatory modules. In addition, ncRNAs, mainly composed of miR-590-3p, miR-495-3p, miR-186-5p, and
transcription factors such as MYC, BRCA1, and CDX2, significantly regulate
COPD dysfunction blocks. In summary, we revealed that the
COPD-related target gene CUL1 plays a key role in the potential dysfunction of the disease. It promotes the proliferation of fibroblast cells in
COPD patients by mediating functional signals of organelle fission and thus participates in the progress of the disease. Our research helps biologists to further understand the etiology and development trend of
COPD.