Asiatic Acid (AA) Sensitizes Multidrug-Resistant Human Lung Adenocarcinoma A549/DDP Cells to Cisplatin (DDP) via Downregulation of P-Glycoprotein (MDR1) and Its Targets.
Role of P-glycoprotein in accumulation and cytotoxicity of amrubicin and amrubicinol in MDR1 gene-transfected LLC-PK1 cells and human A549 lung adenocarcinoma cells.
The study was undertaken to clarify the relationship of the 190k protein to MRP gene expression in non-P-glycoprotein-containing MDR cells of the large-cell and adenocarcinoma lung cancer lines, COR-L23 and MOR.
ClC-3 was highly expressed in the P-glycoprotein (P-gp)-dependent human lung adenocarcinoma cell line (A549)/paclitaxel (PTX) and the human breast carcinoma cell line (MCF-7)/doxorubicin (DOX) resistant cells.
The current study demonstrated that common polymorphisms in the 3' untranslated region of ABCB1 and ABCC1 may contribute to the etiology of lung cancer, providing further support for the hypothesis that genetic components in the metabolism and the disposition of NNK may modify the risk of lung cancer, especially in lung adenocarcinoma among women.
Identification of chromosomal loci associated with non-P-glycoprotein-mediated multidrug resistance to topoisomerase II inhibitor in lung adenocarcinoma cell line by comparative genomic hybridization.
The ability of the nanoparticle to overcome multi-drug resistance was evaluated by the expression of multidrug-resistant proteins P-glycoprotein (P-gp) and Breast cancer resistant protein (BCRP) in lung adenocarcinoma resistant cells (A549<sup>R</sup>).
More importantly, Ad5GS3 exerted potent oncolytic activity against clinical advanced lung adenocarcinoma, which was associated with elevated levels of nuclear YB-1 and cytoplasmic MDR1 expression in the advanced tumors.
In this study, the major purpose was to assess the expression and methylation levels of ABCB1 in human lung adenocarcinoma and to reveal the relationship between these processes and acquisition of cisplatin (DDP) resistance in the human cancer cell line A549.
Furthermore, MRP expression in 4 squamous-cell carcinomas (L13, 18, 19 and 20) was more than 3.6 times higher than in KB-3-1 cells, and the average MRP mRNA expression level of all squamous-cell carcinomas was significantly higher than that of adenocarcinoma of the lung and of colorectal and gastric carcinomas.
In this study, using human lung adenocarcinoma A549 cells as a cell culture model, we demonstrated that an adenosine triphosphate binding cassette (ABC) transporter, ABCG2, was significantly increased by As<sub>2</sub>O<sub>3</sub> treatment, while other ABC transporters, ABCB1 and ABCC1 showed no remarkable change in the response to As<sub>2</sub>O<sub>3</sub>.
The study was undertaken to clarify the relationship of the 190k protein to MRP gene expression in non-P-glycoprotein-containing MDR cells of the large-cell and adenocarcinoma lung cancer lines, COR-L23 and MOR.
The current study demonstrated that common polymorphisms in the 3' untranslated region of ABCB1 and ABCC1 may contribute to the etiology of lung cancer, providing further support for the hypothesis that genetic components in the metabolism and the disposition of NNK may modify the risk of lung cancer, especially in lung adenocarcinoma among women.
We investigated the association between two biomarkers of East Asian ancestry, the genetic polymorphisms ectodysplasin A receptor gene (EDAR) V370A and ATP binding cassette subfamily C member 11 gene (ABCC11) G180A, and the frequency of EGFR mutations in patients with lung adenocarcinoma in a range of countries.
The lung adenocarcinoma (LUAD) cell line A549 was transduced with lentiviral packaging vectors overexpressing either wild-type ABCE1 or ABCE1 with Fe-S cluster deletions (ΔABCE1).
Our results demonstrated the potential role of ABCE1 in human lung adenocarcinoma, which may provide some molecular basis for the mechanisms of development and progress of human lung adenocarcinoma, and help to find new pharmacological targets.
Cisplatin induced HOXB13 expression in lung adenocarcinoma cells, and patient-derived xenografts and depletion of ABCG1 enhanced the sensitivity of lung adenocarcinoma cells to cisplatin therapy.
We investigated the expression of the SHH ligand and its downstream molecules, such as glioma-associated oncogene homologue (GLI)-1, GLI-2, GLI-3, and ATP-binding cassette G2 (ABCG2), in 166 cases of surgically resected lung adenocarcinoma by immunohistochemistry.