Project description:Sepantronium bromide (YM155), a transcriptional inhibitor of anti-apoptotic protein survivin, is considered as a potential drug candidate for triple negative breast cancers (TNBC). Regardless of its excellent performance in pre-clinical models of TNBC, in patients, this drug was unable to outperform the standard chemotherapy docetaxel. The goal of this study was to identify the pathways/molecules affected by YM155 in TNBC cell lines. Detailed biochemical analysis of the paired YM155-sensitive and resistant cell lines indicates that induction of mitochondrial oxidative stress is a first-line response to the drug, ultimately leading to growth inhibition and induction of cell death. Multiple pathways involved in dampening oxidative stress-induced damages are differentially regulated in YM155-resistant cells. Furthermore, the emergence of YM155 resistance is associated with an extensive transcriptional reprogramming and alteration of many more biological pathways in addition to those identified by biochemical assays. Molecules associated with these biological pathways will potentially serve as biomarkers predicting YM155 sensitivity in TNBC cells.
Project description:Precision Run-On Sequencing (PRO-seq) was performed on triple negative breast cancer (TNBC) cell lines and drug resistant cell lines to determine the epigenetic factors that contribute to TNBC subtypes and drug resistance.
Project description:Our preliminary data found that TNBC cells with Chrom 17p loss are more resistant to chemotherapy drug treatment, compare to cell with 17p intact.To investigate the role of cancer stemness, weg performed this gene expression profiling analysis
Project description:Our preliminary data found that TNBC cells with Chrom 17p loss are more resistant to chemotherapy drug treatment, compare to cell with 17p intact.To investigate the role of cancer stemness, weg performed this gene expression profiling analysis
Project description:Cholangiocarcinoma (CCA) poses a significant health challenge, especially in Asian countries. Late-stage diagnoses limit the availability of curative surgical options, underscoring the crucial role of chemotherapy. However, drug resistance presents a formidable obstacle, resulting in recurrent tumors. Despite the revolutionary impact of proteomics on cancer research, the exploration of drug-resistant mechanisms in CCA remains unexplored. In this study, we established 5-fluorouracil (5-FU)- and gemcitabine-resistant CCA cell lines, KKU-213FR and KKU-213GR, derived from the KKU-213A parental line. These cell lines exhibited robust drug resistance, heightened migration, and invasion capabilities.
Project description:Gene expression profiles were performed on MDA-MB-231 TNBC cell line treated with entinostast, all-trans retinoic acid (ATRA), and doxorubicin as single, double, and triple combinations using Illumina. Treatment signatures were made from each drug treatment and integrated to find a comprehensive view of changes associated with the epigenetic, differentiation and chemotherapy combination
