Project description:To determine the drug target of lenvatinib, RNAseq was used to evaluate the transcriptome differences between lenvatinib-treated MHCC-97H cells and their parental counterparts.Results show that SERPINE1 may be direct target of lenvatinib, and AKR1C1 have potential prognostic significance in the prediction of LR(lenvatinib-resistant) in HCC. AKR1C1 could be a promising therapeutic target for patients with LR-type liver cancer.
Project description:RNA sequencing data of paired parental and therapy resistant cancer cell lines. Parental cell lines are mostly established cell lines. Resistant cell lines were obtained through long term exposure of the parental cells to gradually increasing doses of cancer therapies. Samples include 7 parental and 10 derived resistant cell lines. Our aim was to assess whether the resistant cells had undergone Epithelial to Mesenchymal Transition upon resistance acquisition.
Project description:Using a kinome-centred CRISPR/Cas9 genetic screen, we identify here that inhibition of the epidermal growth factor receptor (EGFR) is synthetic lethal with lenvatinib in liver cancer cells. We found that the combination of the EGFR inhibitor gefitinib and lenvatinib displays potent anti-proliferative effect in HCC cell lines that express EGFR in vitro and of xenografted HCC cell lines or patient-derived HCC tumours in mice. Herre, we analyzed the different transcriptome profiling of HCC cells treated with DMSO, lenvatinib, gefitinib, and lenvatinib plus gefitinib by RNA-sequencing.
Project description:To investigate the mechanism of lenvatinib resistance, we established the lenvatinib resistant Huh7 (Huh7 LR) cells by continuous exposuring to lenvatinib (1–20 μM) for approximately 10 months. We then performed gene expression profiling analysis using data obtained from RNA-seq of Huh7 parental (Huh7 P) cells and the lenvatinib resistant Huh7 (Huh7 LR) cells.
Project description:To better identify the key gene involved in sorafenib-resistant HCC cells and uncover potential targets for HCC therapy, the microarray analysis was used to screen the differentially expressed genes in sorafenib-resistant HCC cells, xenograft model and the corresponding counterparts.
Project description:RNA transcriptome sequencing analysis was performed in SNU-668 Erastin-resistant cells and SNU-668 parental cells, SNU-484 RSL3-resistant cells and SNU-484 parental cells
Project description:Parental and AqR cells were obtained at diferent time-points (Day1 and Day 18). Total RNA was extracted and submitted for RNA-seq. Differential expression was observed between parental and AqR cells. AqR cells were derived from parental cells by adding inhibitor (CAY10566) every 3 days until cells became resistant (at about 3 weeks).
Project description:RNA sequencing data of paired parental and therapy resistant cancer cell lines. Parental cell lines are mostly established cell lines. Resistant cell lines were obtained through long term exposure of the parental cells to gradually increasing doses of cancer therapies. Samples include 7 parental and 10 derived resistant cell lines. Our aim was to assess whether the resistant cells had undergone Epithelial to Mesenchymal Transition upon resistance acquisition and whether EMT disappears upon knock down of the DNMTs