ABSTRACT: Gene expression microarray and CGH array of metabolically adaptable cells derived from SUM149 triple-negative Inflammatory Breast Cancer cell line
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: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:aCGH: Human SUM149-Luc triple-negative Inflammatory Breast Cancer cell line versus its metabolically adaptable variants MA1 and MA2
Project description: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 used gene expression microarrays 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 MA1 and MA2 variants to a common parental cell line SUM149-Luc. One sample each.
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: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 used gene expression microarrays 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:In order to identify state changes that mediate the transition from sensitive to a resistant cell states, we applied RNA velocity analysis to an existing single-cell RNAseq (scRNAseq) dataset of BRD4 inhibitor sensitive and resistant SUM149 and SUM159 triple negative breast cancer cell lines. Both SUM149 and SUM159 cell lines treated with or without JQ1 had similar cell communities and trajectories including a stem cell-like and embryonic diapause (SCLED) cell state, a transiting cell state and a number of drug resistant states. Interestingly a transcriptional signature derived from the transiting state but not the SCLED state was associated with worsened outcomes in basal-like breast cancer patients as well as with a micrometastasis signature suggesting that the ability to transit from the SCLED state to drug resistant states could contribute to patient outcomes. The shift from the SCLED state to a transiting cell state was characterized by elevated expression of the CD9 tetraspanin. CD9 knockdown sensitized SUM149 tumor cells to JQ1 in vitro and in vivo trapping cells in the SCLED state and limiting transit to resistant cell states. CD9 knockdown sensitized SUM149 to multiple additional cytotoxic drugs suggesting a generalized role in drug resistance. Thus, CD9 appears to be critical for the ability of triple negative breast cancer cells to escape from a stem cell-like/embryonic diapause state and transition into a treatment resistant state.
Project description:Five Triple Negative Breast Cancer cell lines were exposed to increasing concentration of Paclitaxel untill they acquired resistance. In order to identify changes in gene expression associated with resistance to PTX, we performed gene expression profiling on parental and resistant cell lines. Of ~22000 genes surveyed by microarray analysis, 5.0%, 3.7%, 9.0%, 7.3%, and 5.4% of the genes showed changes in expression of 2-fold or greater (p value < 0.05) in BT20, SUM149, MDA-MB-231, MDA-MB-436 and MDA-MB-468 cell lines, respectively.