Lung cancer is a malignant tumor that originates in the bronchial mucosal epithelium or alveolar epithelium, with non-small cell lung cancer (NSCLC) accounting for approximately 85 % of lung cancer, and lung adenocarcinoma (LUAD) accounting for the majority of cases.1 It is reported that lung cancer is the malignant tumor with the highest incidence rate and the highest number of deaths in the world.2 Due to many factors such as the low effectiveness of screening programmers, the late onset of clinical symptoms, etc. Most lung cancer patients are diagnosed in the middle and late stages with a poor prognosis. Advanced LUAD patients lose the opportunity for surgical treatment, and drug therapy is the main means of treating lung cancer.3 In recent years, significant progress has been made in targeted therapy and immunotherapy, but the overall 5-year survival rate for lung cancer is only 15 %.4 Therefore, a detailed exploration of the molecular mechanisms of lung cancer and increased drug sensitivity are crucial to improve lung cancer prognosis.

Gemcitabine is a pyrimidine nucleotide analogue, which belongs to the category of antimetabolic anticancer drugs.5 It is also a first-line drug for advanced non-small cell lung cancer such as lung adenocarcinoma.6 With the widespread application of gemcitabine in clinical practice, tumor resistance is also known to be a key issue restricting the clinical efficacy of gemcitabine.7 Numerous genes have been reported to be involved in the development of resistance to gemcitabine. In a bioinformatic analysis study of hepatocellular carcinoma (HCC), it was discovered that mitotic checkpoint serine/threonine-protein kinase BUB1 beta (BUB1B) is associated with a poor prognosis and resistance to gemcitabine in HCC.8 In another study of gemcitabine-resistant bladder cancer, the expression level of BUB1B was found in the T24 gemcitabine resistant cell line.9 These pieces of evidence suggest that BUB1B may be involved in the development of resistance to gemcitabine. However, currently there is no report on whether the expression level of BUB1B in lung cancer affects resistance to gemcitabine and the specific mechanism.

Therefore, this study aims to explore the expression of BUB1B in lung adenocarcinoma and observe the effect of BUB1B on the resistance of gemcitabine in lung adenocarcinoma to provide new aspects to increase the sensitivity of the gemcitabine drug.