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Lung adenocarcinoma (LUAD) is one of the most common and malignant cancer types. Abnormal cell proliferation, exemplified by cell cycle and cell division dysregulation, is one of the most prominent hallmarks of cancer and is responsible for recurrence, metastasis, and resistance to cancer therapy. However, LUAD-specific gene regulation and clinical significance remain obscure. Here, by using both tissues and cells from LUAD and normal lung samples, 434 increased and 828 decreased genes of biological significance were detected, including 127 cell cycle-associated genes (95 increased and 32 decreased), 66 cell division-associated genes (56 increased and 10 decreased), and 81 cell proliferation-associated genes (34 increased and 47 decreased). Among them, 12 increased genes ( TPX2 ,  CENPF ,  BUB1 ,  PLK1 ,  KIF2C ,  AURKB ,  CDKN3 ,  BUB1B ,  HMGA2 ,  CDK1 ,  ASPM , and  CKS1B ) and 2 decreased genes ( TACC1  and  MYH10 ) were associated with all the three above processes. Importantly, 2 ( CDKN3  and  CKS1B ) out of the 11 increased genes (except  HMGA2 ) are previously uncharacterized ones in LUAD and can potentially be prognostic markers. Moreover,  PLK1  could be a promising therapeutic target for LUAD. Besides, protein–protein interaction network analysis showed that  CDK1  and  CDC20  were the hub genes, which might play crucial roles in cell proliferation of LUAD. Furthermore, transcriptional regulatory network analysis suggested that the transcription factor E2F1 could be a key regulator in controlling cell proliferation of LUAD  via  expression modulation of most cell cycle-, cell division-, and cell proliferation-related DEGs. Finally, trichostatin A, hycanthone, vorinostat, and mebeverine were identified as four potential therapeutic agents for LUAD. This work revealed key regulators contributing to cell proliferation in human LUAD and identified four potential therapeutic agents for treatment strategy.

A Systematic Analysis Identifies Key Regulators Involved in Cell Proliferation and Potential Drugs for the Treatment of Human Lung Adenocarcinoma