These variants were mainly involved in DNA repair (EXCC1, XPA, XPD, XPG, XRCC1 and XRCC3), drug influx and efflux (MDR1), metabolism and detoxification (GSTP1) and DNA synthesis (MTHFR), and might be considered as potential prognostic biomarkers for assessing objective response and progression risk in NSCLC patients receiving platinum-based regimens.
The potential applications for this finding are provided evidence to screen the potential P-gp reversors and to diagnose and manage the chemoresistance in NSCLC patients.
The results of the present study indicated that β-ELE could reverse drug resistance in erlotinib-resistant human NSCLC A549/ER cells <i>in vitro</i> through a mechanism that may involve the decreased expression of P-gp, inhibition of P-gp dependent drug efflux and the increased intracellular concentration of anticancer drugs.
This study aimed to investigate the role of long non-coding RNA (lncRNA) X-inactive specific transcript (XIST) and multidrug resistance-1 (MDR1) in tumor tissue samples and the chemoresistant human NSCLC cell lines, H460/DDP and A549/DDP, and in a murine A549/DDP tumor xenograft.
A panel of 17 non-small cell lung cancer (NSCLC) cell lines was used to investigate whether alterations in the ABCB1 gene or its mRNA expression correlated with in vitro chemosensitivity to paclitaxel.
Here, we assessed relationships between CXC chemokine receptor type 4 (CXCR4) and focal adhesion kinase (FAK) gene expression levels and expression levels of the drug resistance-related genes ABCB1 and ABCC1, and tested the potential of CXCR4 and FAK inhibitors to reverse doxorubicin (DOX) resistance and to decrease the invasive capacity of non-small cell lung carcinoma (NSCLC) cells.
In addition, compared with the adjacent normal lung tissue, the levels of CSC‑associated biomarkers CD133, OCT4A, NANOG and MDR1 were significantly increased in NSCLC tissue.
Gene expression data confirmed the induction of mdr1 (P-gp), as judged by the observed 15-fold increase in its mRNA concentration in doxorubicin-resistant NCI-H460/R cells.
The aim of this study was to investigate prognostic value of multidrug resistance protein 1 (MRP1), breast cancer resistance protein (BCRP), lung resistance-related protein (LRP) and excision repair cross-complementing 1 (ERCC1) in patients with locally advanced non-small cell lung cancer (NSCLC) who received neoadjuvant cisplatin-based chemotherapy.
We performed this meta-analysis to compare outcome to platinum-based chemotherapies in advanced non-small cell lung cancer (NSCLC) with different ERCC1 C118T/C8092A and MDR1C3435T polymorphisms.
However, P-gp and GST-pi showed no significant relationship with either response rate or survival in patients with unresectable NSCLC receiving CDDP-based chemotherapy.
Our data demonstrate that CHD1L could induce cisplatin resistance in NSCLC via c-Jun-ABCB1-NF-κB axis, and may serve as a novel predictive marker and the potential therapeutic target for cisplatin resistance in NSCLC.
In this study, we have investigated whether polymorphisms in genes that control import/export of drugs (MDR1) and that repair DNA adducts (ERCC1) are involved with drug resistance in non-small cell lung cancer (NSCLC) patients.
Our findings suggest that the MDR1 2677G>T/A polymorphism and the 2677G-3435C haplotype are predictors of treatment response to docetaxel-cisplatin chemotherapy in NSCLC patients.
MDR1 RNA levels were usually elevated in untreated, intrinsically drug-resistant tumors, including those derived from the colon, kidney, adrenal gland, liver, and pancreas, as well as in carcinoid tumors, chronic myelogenous leukemia in blast crisis, and cell lines of non-small cell carcinoma of the lung (NSCLC) with neuroendocrine properties.
Future studies of mdr1 and mrp1 using increased-sensitivity qPCR techniques, in parallel with protein analysis, in larger cohorts of cases may help to elucidate the role of drug efflux pumps in NSCLC multiple drug resistance.