Project description:ARID1A has been suggested as a key regulator for anti-tumor immunity. In the present study, we evaluated the role of ARID1A deficiency in inducing adaptive immune resistance in triple negative breast cancer. To investigate global chromatin remodeling, we performed ATAC–seq in ARID1A knockout and control MDA-MB-231 cells.
Project description:ARID1A has been suggested as a key regulator for anti-tumor immunity. In the present study, we evaluated the role of ARID1A deficiency in inducing adaptive immune resistance in triple negative breast cancer. Next-generation sequencing analysis was performed in control and ARID1A knockout MDA-MB-231 cells to investigate global gene expression changes.
Project description:ARID1A has been suggested as a key regulator for anti-tumor immunity. In the present study, we evaluated the role of ARID1A deficiency in inducing adaptive immune resistance in triple negative breast cancer. To explore global transcriptional activity, we performed chromatin immunoprecipitation followed by high-throughput sequencing (ChIP–seq) to investigate H3K4me3 histone modification of ARID1A knockout and control MDA-MB-231 cells.
Project description:ARID1A has been suggested as a key regulator for anti-tumor immunity. In the present study, we evaluated the role of ARID1A deficiency in inducing adaptive immune resistance in triple negative breast cancer. To explore global transcriptional activity, we performed chromatin immunoprecipitation followed by high throughput sequencing (ChIP–seq) to investigate H3K27ac histone modification of ARID1A knockout and control MDA-MB-231 cells.
Project description:ARID1A has been suggested as a key regulator for anti-tumor immunity. In the present study, we evaluated the role of ARID1A deficiency in inducing adaptive immune resistance in triple negative breast cancer. To explore global transcriptional activity, we performed chromatin immunoprecipitation followed by high throughput sequencing (ChIP–seq) to investigate H3K4me1 histone modification of ARID1A knockout and control MDA-MB-231 cells.