Project description:Although membrane-anchored PD-L1 has been well-studied for its engagement with PD-1 on T cells to evade anti-tumor immunity, whether PD-L1 regulate oncogenic signaling pathways in tumor cells remains elusive. Methods: Total RNA from MDA-MB-231 wild type (WT) , MDA-MB-231 PD-L1 knock-out (KO), CT26 WT or CT26 Pd-l1 KO cells was purified using Qiagen RNeasy mini kit (Qiagen) according to the manufacturer’s instructions. Library preparation and sequenceing analysis were performed at the Molecular Genetics Core facility in Dana-Farber Cancer institute. RNA-seq data was aligned using STAR v2.5.4a. Conclusions: Our study indicates that PD-L1 may regulate genes that are involved in immune response regulating pathways.
Project description:Analysis of MDA-MB-231 breast cancer cells overexpressing lncRNA neuroblastoma associated transcript 1 (NBAT1). Results provide insight into the function of NBAT1 in breast cancer. NBAT1 overexpressed in breast cancer cells MDA-MB-231 compared to control (empty vector alone). Three replicates of each treatment were analyzed.
Project description:Aurora Kinase B and ZAK interaction model
Equivalent of the stochastic model used in "Network pharmacology model predicts combined Aurora B and ZAK inhibition in MDA-MB-231 breast cancer cells" by Tang et. al. 2018.
The only difference is cell division and partitioning of the components, which are available in the original model for SGNS2.
Project description:Analysis of MDA-MB-231 breast cancer cells overexpressing lncRNA neuroblastoma associated transcript 1 (NBAT1). Results provide insight into the function of NBAT1 in breast cancer.
Project description:Although membrane-anchored PD-L1 has been well-studied for its engagement with PD-1 on T cells to evade anti-tumor immunity, whether PD-L1 regulate oncogenic signaling pathways in tumor cells remains elusive. We found that a portion of PD-L1 could translocate to the nucleus and knockout of PD-L1 changed RNA profiles in MDA-MB-231 cells. To further explore potential role of PD-L1 in regulating gene expression in tumor cells, we performed ChIP-seq in HA tag-inserted (after the signal peptide) PD-L1 re-expressed MBA-MB-231cells (endogenous PD-L1 knockout background). Methods: HA-insert-PD-L1 was re-introduced into MDA-MB-231 PD-L1 knockout cells using lentivirus and then the infected cells were selected with puromycin to make stable subclones. ChIP experiments were performed using HA antibody (Abcam, ab9110). Conclusions: Our study indicates that nuclear PD-L1 has potential roles in regulating gene transcription. More efforts are needed to further dissect the exact working model.
Project description:The cytokine Oncostatin M (OSM) promotes cancer progression by acting as central node for multicellular interactions between cancer cells and surrounding stromal cells. OSM is mainly secreted by myeloid cells and the oncostatin M receptor (OSMR) is expressed by cancer cells and cancer associated fibroblasts (CAFs), among others. To understand the effect of OSM in triple negative breast cancer cells, a small and well-annotated Clariom S gene microarray was performed in OSM-overexpressing (MDA-MB-231-hOSM) and control (MDA-MB-231-hC) MDA-MB-231 cells.
Project description:The project profiled the expression patterns in hypoxia induced secretomes between MDA-MB-231 parental and MDA-MB-231 Bone Tropic (BT) breast cancer cell lines which have been previously generated by Massague and colleagues (Kang et al. Cancer Cell 2003).
