Breast Cancer Initiating Cells RNA-seq
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Similar Datasets
Project description:We previously reported the isolation and in vitro propagation of highly tumorigenic mammospheres (MCFS) isolated from MCF7 breast cancer cell line. In this study we obtained gene expression profiles of MCFS and parental MCF7 cell lines using SOLiD RNA-sequencing after linear isothermal DNA amplification.
2015-11-13 | E-MTAB-2811 | biostudies-arrayexpress
Project description:Bulk cancer cell populations are known to display distinct metabolic properties compared to their normal counterparts. However, relatively little is known about heterogeneity of metabolic properties within tumors. In this study we show that, analogous to some normal stem cells, breast tumor initiating cells (TICs, also called cancer stem cells) have distinct metabolic properties compared to non-tumorigenic cancer cells (NTCs). Transcriptome profiling using RNA-Seq revealed TICs under-express genes involved in mitochondrial oxidative phosphorylation and although TICs are relatively quiescent, they preferentially perform glycolysis over oxidative phosphorylation compared to NTCs. TICs contain fewer mitochondria and display lower expression and activity of pyruvate dehydrogenase (Pdh), a key regulator of oxidative phosphorylation. Metabolic reprogramming of TICs by pharmacologic activation of Pdh preferentially eliminates TICs in vitro and in vivo. Our findings reveal unique metabolic properties of TICs and indicate that metabolic reprogramming represents a promising strategy for targeting these cells. Examination transcriptome profiles for breast tumor initiating cells (TICs) and non-tumorigenic cells (NTCs)
2014-07-31 | E-GEOD-41286 | biostudies-arrayexpress
Project description:RNA-seq was performed on breast cancer cell lines and primary tumors RNA-seq was performed on 28 breast cancer cell lines, 42 Triple Negative Breast Cancer (TNBC) primary tumors, and 42 Estrogen Receptor Positive (ER+) and HER2 Negative Breast Cancer primary tumors, 30 uninovlved breast tissue samples that were adjacent to ER+ primary tumors, 5 breast tissue samples from reduction mammoplasty procedures performed on patients with no known cancer, and 21 uninvolved breast tissue samples that were adjacent to TNBC primary tumors.
2014-06-11 | E-GEOD-58135 | biostudies-arrayexpress
Project description:We have generated tumorigenic (S2N) and non-tumorigenic (S2), normal-like to basal-like breast cancer cell lines from primary tumors. At high in vivo inoculation cell numbers of 10^6 cells/mouse both S2N and S2 monolayer as well as sphere culture cells grew at similar rates. However, at low inoculation cell numbers down to 10^3 cells only S2N sphere cells generated xenograft tumors. mRNA profiling revealed a unique cluster pattern of the tumorigenic S2N sphere cells, but a detailed analysis of TIC relevant transcription factors like Oct3, Sox and Nanog family members, Myc, Slug or Twist1 revealed no consistently increased expression in the highly tumorigenic cell lines. Our data indicate that the intrinsic genetic and functional markers investigated are not solely indicative of the in vivo tumorigenicity of putative breast tumor-initiating cells. 4 samples with 3 replicates each
2012-12-21 | E-GEOD-32526 | biostudies-arrayexpress
Project description:RNA-seq analysis of breast cancer
| PRJNA453538 | ENA
Project description:Breast Cancer - immune clusters - RNA-seq
| PRJNA558331 | ENA
Project description:MMP14 empowers tumor-initiating breast cancer cells under hypoxic nutrient-depleted conditions
| PRJNA454197 | ENA
Project description:We have generated tumorigenic (S2N) and non-tumorigenic (S2), normal-like to basal-like breast cancer cell lines from primary tumors. At high in vivo inoculation cell numbers of 10^6 cells/mouse both S2N and S2 monolayer as well as sphere culture cells grew at similar rates. However, at low inoculation cell numbers down to 10^3 cells only S2N sphere cells generated xenograft tumors. mRNA profiling revealed a unique cluster pattern of the tumorigenic S2N sphere cells, but a detailed analysis of TIC relevant transcription factors like Oct3, Sox and Nanog family members, Myc, Slug or Twist1 revealed no consistently increased expression in the highly tumorigenic cell lines. Our data indicate that the intrinsic genetic and functional markers investigated are not solely indicative of the in vivo tumorigenicity of putative breast tumor-initiating cells.
2012-12-21 | GSE32526 | GEO
Project description:The erythropoietin (EPO) hormone induces red blood cell production and its recombinant form is the most prescribed drug for the treatment of anemia, including that arising in cancer patients. Based on randomized trials showing that EPO administration to cancer patients result in a decreased survival, we investigated the impact of EPO modulation on tumorigenesis. Using genetically engineered mouse models of breast cancer we found that EPO promoted tumorigenesis by activating JAK/STAT signaling specifically in breast tumor initiating cells (TICs) and promoting their self-renewal. Moreover, we define an active role for endogenous EPO in breast cancer progression and breast TIC self-renewal and demonstrate a potential application of EPO pathway inhibition in breast cancer therapy. reference x sample
2014-05-31 | E-GEOD-51433 | biostudies-arrayexpress
Project description:The erythropoietin (EPO) hormone induces red blood cell production and its recombinant form is the most prescribed drug for the treatment of anemia, including that arising in cancer patients. Based on randomized trials showing that EPO administration to cancer patients result in a decreased survival, we investigated the impact of EPO modulation on tumorigenesis. Using genetically engineered mouse models of breast cancer we found that EPO promoted tumorigenesis by activating JAK/STAT signaling specifically in breast tumor initiating cells (TICs) and promoting their self-renewal. Moreover, we define an active role for endogenous EPO in breast cancer progression and breast TIC self-renewal and demonstrate a potential application of EPO pathway inhibition in breast cancer therapy.
2014-05-31 | GSE51433 | GEO