## 1 Introduction
The first transporter from this family that was identified was P-glycoprotein (P-gp), which has since remained the most studied and most important transporter involved in multidrug resistance (MDR). Due to the wide substrate spectrum, P-gp protects the cellular environment by pumping out numerous xenobiotics of exogenous origin and endogenous ligands, and it also inhibits the transport of compounds through the blood-brain, blood-tesis, and blood-placental barriers, while its overexpression leads to the formation of MDR [13]. This phenomenon can be the cause of chemotherapy failure. Inhibitors of this protein are being intensively studied in terms of limiting MDR: from the early generation of P-gp inhibitors with significant toxicity, through newer generations characterized by unsatisfactory clinical effectiveness, to other drugs showing anti-cancer properties and, e.g., mTOR kinase inhibitors that indirectly inhibit P-gp [14,15]. The amount of the transporter in cancer cells may be increased as a result of chemotherapy and the acquisition of resistance to the compounds used as P-gp substrates. However, it has been observed that the process of carcinogenesis itself may be associated with a change in the amount of protein in cells undergoing neoplastic transformations. In the case of cancers of organs in which cells in the physiological state are characterized by high expression of P-gp, i.e., the kidneys or liver, the amount of synthesized protein becomes even greater. On the other hand, in cancers that affect other organs, including the lungs, where the transporter is physiologically at a lower level ([[https://www.ncbi.nlm.nih.gov/gene/5243](https://www.ncbi.nlm.nih.gov/gene/5243)]([https://www.ncbi.nlm.nih.gov/gene/5243](https://www.ncbi.nlm.nih.gov/gene/5243)), accessed on 15 May 2023), the amount of protein decreases as the disease progresses [16]. P-glycoprotein is encoded by the polymorphic gene \(ABCB1\) (ATP-Binding Cassette Subfamily B Member 1). One of the best-known polymorphisms of this gene is SNP C3435T (rs1045642), which probably affects the transcript level and consequently the amount of protein [17]. Similar correlations were also investigated for other polymorphisms of this gene located in the coding region, introns, and the promoter region [18]. The biological and clinical effects that are associated with these polymorphisms may be the consequences of alternative mRNA splicing, changes in its structure or stability, and modifications in translation kinetics involving rare tRNAs recognizing a modified codon. \(ABCB1\) gene expression can also be modulated by factors such as heat shock, cytokines, chemotherapeutics, UV radiation, oxygen free radicals, and numerous transcription factors that can regulate expression post-transcriptionally by affecting mRNA maturation. Moreover, the p53 protein can positively and negatively affect \(ABCB1\) transcription [19]. The regulatory sequences of the promoter region, which are located upstream of the transcription start site and contain CpG islands that can undergo methylation, are also important elements that modulate the expression of \(ABCB1\)[20]. All these observations suggest that different levels of expression of the P-gp gene should be expected in cancer cells, including lung cancer cells. Therefore, the aim of the study was to assess the clinical significance of the \(ABCB1\) gene in patients with lung cancer using data collected in selected bioinformatics databases. The levels of expression and methylation of the \(ABCB1\) gene in normal and neoplastic lung tissues were analyzed, taking into account their potential correlations with clinicopathological and molecular parameters of the disease.