Project description:SUM149 breast cancer cells were treated with NRAD1 gapmers for 48 hrs and RNA was extracted. RNA was analysed on affymetrix human transcriptome array 2.0
Project description:Purpose: Transcriptome profiling (RNA-seq) of a novel human Inflammatory Breast Cancer cell line A3250 in comparison to SUM149 and MDA-MB-231 Inflammatory Breast Cancer (IBC) is the most aggressive form of breast cancer with distinct clinical and histopathological features, but understanding of the unique aspects of IBC biology lags far behind that of other breast cancers. We describe a novel triple-negative IBC cell line, A3250, that recapitulates key features of human IBC in a mouse xenograft model.The purpose of this study was to compare differences in gene expression between A3250 IBC, MDA-MB-231 non-IBC and SUM149 IBC that does not present with typical clinical sympotms of IBC in a mouse model, with the goal of identifying unique molecular features for this unique type of breast cancer Results: RNA-Seq analysis identified expression profile characteristic for the novel A3250 IBC cell line, compared to SUM149 IBC and MDA-MB-231 non-IBC.
Project description:Immortalized human breast cancer cell line, SUM149, was analyzed via RT-qPCR for transcript expression of selected cytokines and cytokine receptors associated with promotion of tumor vasculature and breast cancer metastasis
Project description:Inflammatory breast cancer (IBC) is a rare type of breast cancer but accounts for up to 10% of breast cancer-related deaths. Plasticity between epithelial and mesenchymal feature is reported to be crucial in metastasis of IBC. Using Matigel culture, we induced epithelial to mesenchymal transition (EMT) in epithelial-like SUM149 IBC cells and identified overexpressed genes in this EMT process.
Project description:Breast cancer subtype-specific lncRNAs AL078604.2 and LINC01269 were knockdown in breast cancer cell lines LncRNA AL078604.2 was knockdown by an anti-AL076804.2 antisense oligonucleotides (ASOs) in triple-negative breast cancer cell lines MDA-MB-231 and MDA-MB-468 breast cancer cells. LncRNA LINC01269 was knockdown by an anti-LINC01269 ASOs in HER2+ SKBR3 breast cancer cells. To ensure the initial presence of AL078604.2 and LINC01269 in their respective cell lines, qPCR analysis was performed to confirm their expression levels prior to knockdown experiments. The effectiveness of knockdown was confirmed by qPCR analysis, which validated the reduction in AL078604.2 and LNC01269 expression in their corresponding cell lines following ASO treatment.
Project description:CGH array of MA1 and MA2 variant cells as compared to the parental SUM149-Luc breast cancer cell line. The MA1 and MA2 variants were isolated based on the ability of rare cancer cells to survive and grow without adding glutamine in culture medium. To gain insight into the characteristic of metabolically adaptable MA cells that enables them to survive severe metabolic challenge, i.e., prolonged lack of glutamine and other challenges [Singh et al., PLoS ONE 7: e36510, 2012], we analyzed CGH array to compare these cells with the parental SUM149-Luc (luciferase-transfected) cells. We analyzed two independently selected cell populations, one from 0.5 million parental cells (designated MA1) and one from 1 million parental cells (designated MA2). Comparing the MA1 and MA2 variants to the common parental SUM149-Luc cell line. One sample each.
Project description:CGH array of MA1 and MA2 variant cells as compared to the parental SUM149-Luc breast cancer cell line. The MA1 and MA2 variants were isolated based on the ability of rare cancer cells to survive and grow without adding glutamine in culture medium. To gain insight into the characteristic of metabolically adaptable MA cells that enables them to survive severe metabolic challenge, i.e., prolonged lack of glutamine and other challenges [Singh et al., PLoS ONE 7: e36510, 2012], we analyzed CGH array to compare these cells with the parental SUM149-Luc (luciferase-transfected) cells. We analyzed two independently selected cell populations, one from 0.5 million parental cells (designated MA1) and one from 1 million parental cells (designated MA2).
Project description:NRAD1 was knocked down using GapmeRs specific to NRAD1. The breast cancer cells used in this study were confirmed to have NRAD1 expression by qPCR and knockdown of NRAD1 was confirmed by qPCR.