LAUSR

OBJECTIVE Lung adenocarcinoma is an important pathological type of lung cancer. Drug resistance is the main reason for failure of lung adenocarcinoma therapy. The purpose of this study is to explore the role of HOTTIP in the progression of lung adenocarcinoma and in drug resistance. PATIENTS AND METHODS Differentially expressed lncRNAs in normal lung tissues and lung adenocarcinoma tissues were analyzed in The Cancer Genome Atlas (TCGA) database, followed by analysis of differential lncRNAs in treated sensitive and insensitive groups. HOTTIP was found to be highly expressed in lung adenocarcinoma tissues and in drug-resistant tissues. Next, the expression of HOTTIP in clinical samples and its relation to clinical data were analyzed. Then, we examined the effect of HOTTIP in lung adenocarcinoma by detecting changes in cell proliferation and drug resistance after overexpression and interference with HOTTIP. RESULTS By analyzing the normal and lung adenocarcinoma tissues from TCGA database and the treatment of sensitive and insensitive samples, we found that HOTTIP was overexpressed in lung adenocarcinoma and significantly increased in the treatment-insensitive group. Similar results were obtained in clinical samples. In order to explore the role of HOTTIP in lung adenocarcinoma, the proliferation ability of A549 and the drug resistance of A549/PA were significantly reduced after interfering with HOTTIP. Overexpression of HOTTIP, proliferation ability of A549 and drug resistance of A549/PA was significantly enhanced. CONCLUSIONS HOTTIP can promote the progression of lung adenocarcinoma, and the formation of lung adenocarcinoma resistance regulated by the protein kinase B (AKT) signaling pathway.