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PROVIDER: PRJNA338942 | ENA |
REPOSITORIES: ENA
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Project description:miRNA expression of exosomes derived from lung cancer cells A549 and cisplatin (DDP) resistant lung cancer cells A549/DDP
| PRJNA338941 | ENA
Project description:This study aims to identify pathway involvement in the development of cisplatin (cis-diamminedichloroplatinum (II); CDDP) resistance in A549 lung cancer (LC) cells by utilizing advanced bioinformatics software. We developed CDDP-resistant A549 (A549/DDP) cells through prolonged incubation with the drug and performed RNA-seq on RNA extracts to determined differential mRNA and miRNA expression between A549/DDP and A549 cells
2021-05-31 | GSE157692 | GEO
Project description:Silver nanoparticles (AgNPs) have shown great potential as therapeutic agents due to their ability to cause apoptotic cell death in cancer cells. However, little knowledge is available regarding the underlying action mechanisms of AgNPs towards multi-drug resistant cancer cells. Herein, we employed quantitative proteomics to investigate the cytotoxic mechanisms of AgNPs on both cisplatin-sensitive (A549 cells) and -resistant (A549/DDP cells) human lung adenocarcinoma and to explore their potential anticancer abilities. We first performed cytotoxicity tests and found that AgNPs exert similar cytotoxic effects on A549 and A549/DDP cells. At the proteome level, A549 and A549/DDP cells responded to AgNPs distinctively and similarly by causing cell apoptosis via upregulating RNA metabolism, suppressing VEGF siganling pathway, repressing p53-mediated pathways, promoting cell cycle arrest, etc. Additionally, AgNPs remarkably induced ROS generation in A549 and A549/DDP cells. The mitotoxicity results further confirmed the effectiveness of AgNPs in hampering mitochondrial function and respiration in A549 and A549/DDP cells. Overall, our investigations showed that AgNPs could effectively induce cell deaths in human lung adenocarcinoma cells regardless of their sensitivities to cisplatin, suggesting that AgNPs could be potentially used in biomedical aspects as an anticancer agent in alleviating the problem of acquired drug resistance in chemotherapy.
2025-05-30 | PXD064272 | Pride
Project description:Combination therapy as an important treatment option for lung cancer has been attracting attention due to the primary and acquired resistance of chemotherapeutic drugs in the clinical application. In the present study, as a new therapy strategy, concomitant treatment with time-restricted feeding (TRF) plus cisplatin (DDP) on lung cancer growth was investigated in DDP-resistant and DDP-sensitive lung cancer cells. We first found that TRF significantly enhanced the drug susceptibility of DDP in DDP-resistant A549 (A549/DDP) cell line, illustrated by reversing the inhibitory concentration 50 (IC50) values of A549/DDP cells to normal level of parental A549 cells. We also found that TRF markedly enhanced DDP inhibition on cell proliferation, migration, as well as promoted apoptosis compared to the DDP-alone group in A549, H460 and A549/DDP cells lines. We further revealed that the synergistic anti-tumor effect of combined DDP and TRF was greater than that of combined DDP and simulated fasting condition (STS), a known anti-tumor cellular medium. Moreover, mRNA sequence analysis from A549/DDP cell line demonstrated the synergistic anti-tumor effect involved in upregulated pathways in p53 signaling pathway and apoptosis. Notably, compared with the DDP-alone group, combination of TRF and DDP robustly upregulated the P53 protein expression without mRNA level change by regulating its stability via promoting protein synthesis and inhibiting degradation, revealed by cycloheximide and MG132 experiments. Collectively, our results suggested that TRF in combination with cisplatin might be an additional novel therapeutic strategy for patients with lung cancer
2023-01-11 | GSE222187 | GEO
Project description:To investigate the difference of miRNA expression between lung cancer cell A549 and its DDP-resistant cell strain A549/DDP, we have employed miRNA microarray expression to discover the difference expression of miRNAs of A549 cells and A549/DDP. We conducted RT-qPCR to examine the expression levels of top differential expressed miRNAs, namely, miR-197-5p, miR-4443, miR-642a-3p, miR-27b-3p and miR-100-5p, confirming low variability between two methods. The A549/DDP was established from A549 in our laboratory, by exposing A549 to gradually increasing DDP concentrations, until the final concentration at 1μg/ml. To avoid the influence of drug to the A549/DDP cells, they were cultured in a drug-free medium for at least two weeks before gene expression analysis. miRNA expression of A549 and A549/DDP was then analzyed.
2016-08-16 | E-GEOD-85603 | biostudies-arrayexpress
Project description:To investigate the difference of miRNA expression between lung cancer cell A549 and its DDP-resistant cell strain A549/DDP, we have employed miRNA microarray expression to discover the difference expression of miRNAs of A549 cells and A549/DDP. We conducted RT-qPCR to examine the expression levels of top differential expressed miRNAs, namely, miR-197-5p, miR-4443, miR-642a-3p, miR-27b-3p and miR-100-5p, confirming low variability between two methods.
2016-08-16 | GSE85603 | GEO
Project description:Cisplatin resistance is a major cause of poor prognosis in non-small cell lung cancer (NSCLC). Cisplatin-induced lung cancer cell death is associated with ferroptosis, a type of recently identified programmed cell death. Nrf2 is a critical component of the antioxidant system, and its pro-tumorigenic activity in lung cancer has been extensively studied. However, the role of Nrf2 in cisplatin-induced ferroptosis and drug resistance remains elusive. Here, we demonstrate that cisplatin treatment induced ferroptosis in parental A549 lung adenocarcinoma cells, and that this effect was significantly reduced in cisplatin-resistant A549/DDP cells. Knocking down Nrf2 sensitized A549/DDP cells to cisplatin-induced cytotoxicity by enhancing ferroptosis. Moreover, we demonstrated that Nrf2 promotes the expression of HMOX1, and the Nrf2-HMOX1 pathway is critical in mediating the anti-ferroptotic function. Additionally, immunohistochemical analysis of NSCLC specimens indicated that the Nrf2 expression was correlated with HMOX1, and high levels of Nrf2 and HMOX1 were associated with poor patient survival. These findings suggest that the HMOX1-Nrf2 pathway significantly influences treatment outcomes in NSCLC. Ultimately, we demonstrated that treatment with Nrf2 inhibitor ML385 promoted ferroptosis by inhibiting the Nrf2-HMOX1 pathway, restoring cisplatin sensitivity in drug-resistant cells. Our findings provide insights into the mechanism underlying cisplatin resistance and suggests that targeting the Nrf2-HMOX1 pathway enhances cisplatin-induced ferroptosis and improves NSCLC treatment outcomes.
2025-06-17 | GSE288129 | GEO
Project description:Continuous exposure to cisplatin can induce drug resistance to limit efficacy, however, the underlying mechanisms correlated to cisplatin resistance are still unclear. Drug-sensitive A549 cells and cisplatin-resistant A549/DDP cells were used to explore the potential metabolic pathways and key targets associated with cisplatin resistance by integrating untargeted metabolomics with transcriptomics. The results of comprehensive analyses showed that 19 metabolites were significantly changed in A549/DDP vs A549 cells, and some pathways had a close relationship with cisplatin resistance, such as the biosynthesis of aminoacyl-tRNA, glycerophospholipid metabolism, and glutathione metabolism. Moreover, transcriptomics analysis showed glutathione metabolism was also obviously affected in A549/DDP, which indicated that glutathione metabolism played an import role in the process of drug resistance. Meanwhile, transcriptomics analysis suggested the four enzymes related to glutathione metabolism - CD13, GPX4, RRM2B, and OPLAH - as potential targets of cisplatin resistance in NSCLC. Further studies identified the over-expressions of these four enzymes in A549/DDP. The elucidation of mechanism and discovery of new potential targets may help us have a better understanding of cisplatin resistance.
2019-08-12 | PXD013265 | Pride
Project description:Application of cisplatin (DDP) for treating lung cancer is restricted due to its toxicity and drug resistance. In this study, we aimed to examine whether Jinfukang (JFK), an effective herbal medicine against lung cancer, enhances DDP-induced cytotoxicity in lung cancer cells. Morphologically, we observed JFK increases DDP-induced pro-apoptosis in A549 cells in a synergistic manner. Transcriptome profiling analysis indicated that combination of JFK and DDP regulates genes involved in apoptosis-related signaling pathways. Moreover, we found the combination of JFK and DDP produces synergistic pro-apoptosis effect in other lung cancer cell lines NCI-H1975, NCI-H1650 and NCI-H2228. Particularly, we demonstrated AIFM2 is activated by the combined treatment of JFK and DDP, and partially mediate the synergistic pro-apoptosis effect. Collectively, this study gives the first evidence that activation of AIFM2 contributes to induction of pro-apoptosis by combined treatment with JFK and DDP in human lung cancer cells and provides an insight for its potential clinical application in lung cancer treatment.
2016-09-30 | E-MTAB-4671 | biostudies-arrayexpress
Project description:Cisplatin resistance is a major therapeutic challenge in advanced head and neck squamous cell carcinoma (HNSCC). Here, we aimed to investigate the key signaling pathway for cisplatin resistance in HNSCC cells. HNSCC cell lines that were sensitive (HN4 and HN30) or resistant (HN4/DDP and HN30/DDP) to cisplatin were used for this study. Moreover, the cisplatin-resistant human melanoma cell lines (A375/DDP) and human lung cancer cell lines (A549/DDP) have also been established. To identify the role of proteins in the acquisition of cisplatin resistance, we analyzed the abnormally expressed protein via protein mass spectrometry methods (isobaric tags for relative and absolute quantitation, iTRAQ) in cisplatin-sensitive and cisplatin-resistant cancer cells, and found that VN1R5 was highly expressed in cisplatin-resistant cells. Long noncoding RNA lnc-POP1-1 upregulated by VN1R5. To deeply investigate the mechanism by which lnc-POP1-1 affects cisplatin resistance in HNSCC cells, we used RNA pull-down assays followed by mass spectrometry to explore the putative RNA-binding proteins (RBPs) interacting with lnc-POP1-1.
2020-11-28 | PXD022799 |