Project description:Control (DMSO 0.1%; v/v) and 10 M DRB18 were used to treated 5 million A549 lung cancer cells in vitro for 48 hours. The untargeted metabolomics analysis was performed on the cell lysates. The main objective of the study was to determine changes in metabolite abundances in lung cancer after treatment with DRB18, an inhibitor of glucose transporter proteins.
Project description:Objective: Non-small cell lung cancer (NSCLC) is extremely lethal upon metastasis and requires safe and effective systemic therapies to improve a patient’s prognosis. Prodigiosin (PG) appears to selectively and effectively target cancer but not healthy cells. However, PG’s cancer-specific activity has remained elusive until recently. Methods: PG’s cancer-specific performance was compared to Docetaxel (DTX), Paclitaxel (PTX), and Doxorubicin (DOX) against human lung adenocarcinoma (A549) and human small airway epithelial cells (HSAEC). Combination of PG with DTX, PTX, or DOX in a 1:1 ED50 ratio was also evaluated. MTT assay was used to determine the post-treatment cell viability. RNA-sequencing was used for comparative transcriptomics analysis between A549 and HSAEC treated with 1.0μM PG for 24 h. Results: PG reduced A549 cell viability by four-folds greater than HSAEC. In comparison to DTX, PTX and DOX, PG was ∼1.7 times more toxic toward A549, and 2.5 times more protective toward HSAEC. Combination of PG in 1:1 ED50 ratio with DTX, PTX, or DOX failed to exhibit synergistic toxicity toward A549 or protection toward HSAEC. In A549, genes associated in DNA replication were downregulated, while genes directly or indirectly associated in lipid and cholesterol biogenesis were upregulated. In HSAEC, co-upregulation of oncogenic and tumor suppressive genes was observed. Conclusion: An overactive lipid and cholesterol biogenesis could have caused A549’s autophagy while a balancing-act between genes of oncogenic and tumor-suppressive nature could have conferred HSAEC heightened survival. Overall, PG appears to be a smart chemotherapeutic agent that may be both safe and effective for NSCLC patients.
Project description:To seek if ionizing radiation have different biological effect on lung normal cells and cancer cells, we treated lung epithelial cell line BEAS-2B, non-small cell lung cancer cell line A549 and small cell lung cancer cell line H446 with 10 Gy X-ray radiation
Project description:Anticancer drug sagopilone in lung cancer line A549. We performed gene expression analysis of lung cancer cell line A549 treated with sagopilone and paclitaxel. The aim was to analyse gene expression differences between the two drugs in two different concentrations. A549 cells were treated with medium containing either 2.5 nM sagopilone, 40 nM sagopilone, 4 nM paclitaxel or 40 nM paclitaxel, respectively, vehicle (ethanol 0.1%), or were left untreated for 18 hours. The two different concentrations were chosen according the phenotypes they have caused in A549 cells. Treatment with 2.5 nM sagopilone, 4 nM paclitaxel induced an aneuploid cell population, whereas treatment with 40 nM sagopilone and 40 nM paclitaxel induced mitotic arrest.
Project description:Strongly induction of FOSB was observed in a cationic anticancer peptide TP4 treated human A549 lung cancer cell-line, causing obvious cell death. This work aims to address the gene expression profiling upon FOSB overexpression in A549 cell.
Project description:GPX3 has been reported to be involved in antioxidant, anticancer, and anti-inflammation in various studies. It is also known that expression of GPX3 is low in lung cancer tissues. We performed a microarray using three lung cancer cell lines including A549, H1650, and H1975 lung cancer cell lines. Among these, A549 is highly expressed in GPX3 as compared with H1650 and h1975. Microarrays were used to analyze microRNAs showing other expression between A549 and the other two cell lines.
Project description:To determine the signaling networks that are dysregulated in cisplatin-resistant non-small cell lung cancer, noncoding RNA expression data were obtained from, and compared between, the lung adenocarcinoma cell line, A549, and its cisplatin-resistant derivative, A549/CDDP. Noncoding RNA expression data from a cisplatin-sensitive lung adenocarcinoma cancer cell line (A549) were collected and compared to noncoding RNA expression data from a cisplatin-resistant cell line (A549/CDDP). 3 independent experiments were completed for both the sensitive and resistant cell lines.
Project description:To determine the signaling networks that are dysregulated in cisplatin-resistant non-small cell lung cancer, noncoding RNA expression data were obtained from, and compared between, the lung adenocarcinoma cell line, A549, and its cisplatin-resistant derivative, A549/CDDP. Noncoding RNA expression data from a cisplatin-sensitive lung adenocarcinoma cancer cell line (A549) were collected and compared to noncoding RNA expression data from a cisplatin-resistant cell line (A549/CDDP). 3 independent experiments were completed for both the sensitive and resistant cell lines.
Project description:To determine the signaling networks that are dysregulated in cisplatin-resistant non-small cell lung cancer, noncoding RNA expression data were obtained from, and compared between, the lung adenocarcinoma cell line, A549, and its cisplatin-resistant derivative, A549/CDDP.
Project description:Control (DMSO 0.1%; v/v) and 10 µM DRB18 were used to treated 5 million A549 lung cancer cells in vitro for 48 hours. The untargeted metabolomics analysis was performed on the cell lysates. The main objective of the study was to determine changes in metabolite abundances in lung cancer after treatment with DRB18, an inhibitor of glucose transporter proteins.
