Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

13 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Therapy-induced self-renewal of CD133hi cells regulates escape from tumor dormancy and endocrine-resistant metastatic luminal breast cancer

ABSTRACT: HT induces an OXPHOS metabolic editing of ER+ breast cancers, paradoxically establishing HT-driven self-renewal of dormant CD133hi/ERlo cells mediating metastatic progression, which is sensitive to dual targeted therapy In this study, we demonstrated that CD133hi cells can mediate HT resistance and metastatic progression. Using human luminal breast cancer cell lines we have developed an in vivo model of spontaneous metastatic disease recapitulating what is observed in patients. Combining in vivo and in vitro studies we identified a de-novo cancer stem cell population (CSCs) âCD133hi/ERlo/Notch3hi/IL6hiâ, which are generated from non-CSCs via the sustained suppression of ER activity. We provide evidence that an ER-IL6-IL6R-CD133 loop is a mechanism mediating HT-resistance. Cancer cells were isolated from primary tumor and metastases, labeled with anti-CD133/CD44 conjugated antibodies and FACS sorted (gated on GFP, cancer cells).For microarray gene expression profiling and real time PCR (QPCR), we extracted RNA using Trizol (Invitrogen) from FACS sorted tumour derived cells. RNA concentration was determined with a NanoDrop 2000. The samples were prepared according to standard protocols and hybridized them on Affymetrix HG-U133 A 2.0 microarrays. We normalized the data using Microarray Suite 5.0. Differentially expressed genes between groups were identified with fold-change and t-test cut-offs.

ORGANISM(S): Homo sapiens

SUBMITTER: Jeffrey Zhao

PROVIDER: E-GEOD-69280 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Therapy-induced self-renewal of CD133hi cells regulates escape from tumor dormancy and endocrine-resistant metastatic luminal breast cancer

Project description:HT induces an OXPHOS metabolic editing of ER+ breast cancers, paradoxically establishing HT-driven self-renewal of dormant CD133hi/ERlo cells mediating metastatic progression, which is sensitive to dual targeted therapy In this study, we demonstrated that CD133hi cells can mediate HT resistance and metastatic progression. Using human luminal breast cancer cell lines we have developed an in vivo model of spontaneous metastatic disease recapitulating what is observed in patients. Combining in vivo and in vitro studies we identified a de-novo cancer stem cell population (CSCs) “CD133hi/ERlo/Notch3hi/IL6hi”, which are generated from non-CSCs via the sustained suppression of ER activity. We provide evidence that an ER-IL6-IL6R-CD133 loop is a mechanism mediating HT-resistance.

2016-02-09 | GSE69280 | GEO

Identify the cancer stem cells expression characteristics in ovarian and breast cancer

Project description:The identification and characterization of subpopulations of cancer stem cells (CSCs) provide new understandings and possible therapeutic implications in cancer biology. We found the ovarian cancer sphere cells possessed CSCs properties maintained self renewal, drug resistance, and tumorigenesis. Using high-throughput microarray system, we identified common GO terms and pathway signatures significantly enriched in ovarian and breast cancer stem cells. Ovarian and breast cancer cells were cultured in sphere formation conditions, and total RNA from those spheres and conresponding adhered cell was hybridized on Affymetrix microarrays.

2013-11-25 | E-GEOD-43657 | biostudies-arrayexpress

Expression data comparing CD133+ and CD133- B16-F10 melanoma cells

Project description:Cancer stem cells (CSC) were isolated based on the putative stem cell marker CD133. This subset of cells has been shown to have superior tumorigenicity and metastatic ability compared to cells in the non-CSC compartment (i.e. CD133-). We compared microRNA expression profiles of CSCs to non-CSCs to identify disparities in miRNA expression and explore how these miRNAs may provide a selective survival advantage to cancer stem cells.

2019-05-03 | GSE130283 | GEO

Expression data from CSC and Non-CSC of three HCC cell lines

Project description:Hepatocellular carcinoma (HCC) represents the major subtype of liver cancer, characterized with a high rate of recurrence and heterogeneity. Liver cancer stem cells (CSCs) may account for a hierarchical organization of heterogeneous cancer cells. However, how liver CSCs sustain their self-renewal remains largely unknown. We used microarrays to discover the long non-coding RNAs (lncRNAs) expression underlying cell stem cell (CSC) and non cell stem cell (non-CSC) and identified distinct lncRNAs during this process. We sorted CD13+CD133+ and CD13-CD133- cells from Hep3B, Huh7, and PLC/PRF/5 HCC cell lines as liver CSCs and non-CSCs, then hybridized on Affymetrix microarrays. We sought to identify distinct lncRNAs in liver CSCs.

2015-03-05 | E-GEOD-66529 | biostudies-arrayexpress

snoRNA-sequencing analysis of liver cancer stem cells from human samples

Project description:To explore the role of small nucleolar RNA (snoRNA) on self-renewal of liver cancer stem cells (CSCs), we isolated liver CSCs (CD133+CD13+) and Non-CSCs (CD133-CD13-) from huamn liver tumor tissues.

2023-06-30 | GSE233521 | GEO

Metastasis and Survival of Breast Cancer Stem Cells Mediated by Cytoskeleton Remodeling and PI3K/mTOR Signaling transcription factors

Project description:Cancer metastasis is a fetal problem that claims life of over 90% of cancer patients. It is hypothesized that cancer stem cells (CSCs) mediate cancer metastasis and such cells are often resistant to chemotherapy. Studying BRCA1 associated cancers, we found that CSCs form fillopodia and protrusions enriching for active forms of ezrin/radixin/moesin proteins and they have a much higher potential to metastasize than non-CSCs. Microarray analysis indicated that many pathways related to cell adhesion, extracellular matrix and cytoskeleton were differentially regulated in CSCs. Although inhibition of cytoskeleton remodeling by cisplatin treatment retarded CSC motility and cancer metastasis, drug resistant cancers eventually emerge containing markedly increased number of CSCs. This event is at least partially attributed to the activation of PI3K/mTOR signaling, and can be significantly inhibited by the treatment of rapamycin. These results provide strong evidence that cytoskeletal rearrangement and PI3K/mTOR signaling play a distinct role in mediating CSC mobility and viability, and blocking of both pathways in CSCs synergistically inhibits primary and metastatic cancer growth in BRCA1 associated tumors. The sorted subpopulations based upon CD24, CD29 expression were used in the microarray analysis that was performed with 3 independent biologic sample sets.

2012-04-13 | E-GEOD-26621 | biostudies-arrayexpress

Gene expression profiles of pancreatic ductal adenocarcinoma cell lines differently co-expressing cancer stem cell markers

Project description:Pancreatic cancer stem cells (CSCs) have been described as CD24+/CD44+/EpCAM+ or CD133+ cells. However, no study has determined the co-expression of all of these markers in pancreatic ductal adenocarcinoma. Similarly to other combinations of CSC markers, CD24+/ CD44+/EpCAM+/CD133+ phenotype might more accurately identify true pancreatic CSCs. Therefore, we performed a detailed co-expression analysis of CD24, CD44, EpCAM, and CD133 in 3 cell lines derived from primary pancreatic ductal adenocarcinomas (PDACs). Gene expression profiling was applied in order to further investigate the observed differences in proportion of cells that co-expressed CSC markers among the cell lines.

2016-02-29 | E-MTAB-4055 | biostudies-arrayexpress

CD133+ cells contain cancer stem cell-like properties in Malignant Mixed Mullerian Tumor (Carcinosarcoma) of the Uterus

Project description:Cancer stem cells (CSCs) that display tumor-initiating properties have recently been identified. We herein identify and characterize CSCs in human uterine carcinosarcoma, a highly aggressive and therapy-resistant gynecologic malignancy, which is considered to be of mesodermal origin. FU-MMT-1, a cell-line, which was established by us (Emoto M, Cancer 1992) from a patient with uterine carcinosarcoma, was evaluated. FU-MMT-1 contained a high population of CD133, CD44, CD90, and CD29 positive cells. Using the magnetic bead cell separation method, we isolated CD133+ cells, which predominantly form spheres in culture. These CD133+ cells form transplantable tumors in vivo. A qRT-PCR analysis of the genes implicated in stem cell maintenance revealed that CD133+ cells express significantly higher levels of OCT4, NANOG, and BMI-1 than CD133M-oM-<M- cells. Moreover, CD133+ cells showed a high expression of PAX2 and WNT4, which are the essential genes in Mullerian duct formation. The tumor derived from CD133+ cells replicated vimentin, ERM-NM-1, ERM-NM-2, and PR expressionsM-cM-^@M-^@of the parent tumor. These findings suggest that CD133+ FU-MMT-1 cells have the characteristics of CSCs and Mullerian mesenchymal progenitors. CD133+ and CD133- population of FU-MMT-1 cells were analyzed by microarray.

2013-02-10 | E-GEOD-27172 | biostudies-arrayexpress

Cancer stem cells from lobular infiltrating breast tumor metastasize to bone and acquire a gene signature associated to bone tropism

Project description:We investigated the role of breast cancer stem-like cells (CSCs-like), isolated from primary tumor, in promoting bone metastases in a human-in-mice model. Luciferase-transduced CD44+CD24- breast CSCs-like were injected through subcutaneous (SC) and intracardiac (IC) route in nonobese/severe combined immunodeficient (NOD/SCID) mice carrying subcutaneous human bone implants. The implanted bone was viable, active and human neo-vascularization was present. By in vivo luciferase imaging, we monitored tumor growth and detected bone-localized breast CSCs-like, both after SC and IC injection. Bone metastatic lesions were histologically evident, and tumor cells expressed epithelial markers and vimentin. Bone metastatic cells isolated from bone implants showed a CD44-CD24+ phenotype and re-created tumors and bone metastases after injection in secondary mice. A “bone tropism” expression signature was found to distinguish bone-colonizing cells from parental CSCs-like and to persist at subsequent passages also in the absence of surrounding bone tissue. The bone tropism signature displayed significant enrichment in genes discriminating bone metastases of breast cancer from metastases at other organs. Our results demonstrate the ability of breast CSCs-like to promote bone metastasis and provide a CSCs-like bone tropism signature, with potential prognostic value. C10 breast cancer stem-like cells (CSCs-like) were derived as mammospheres from a lobular-infiltrating breast carcinoma (ER+, HER2-). Samples are organized in the following groups: (i) Breast CSCs-like (C10, duplicate); (ii) Luciferase-transduced CSCs-like (C10L, simplicate); (iii) Bone-isolated C10L metastatic cells (C10-bone, duplicate) and subsequently (iv) grown in vitro as spheroids (C10-CSC, simplicate) or (v) re-grown in subcutaneous implants (C10-SC, duplicate).

2013-11-30 | E-GEOD-36102 | biostudies-arrayexpress

Mitochondria help avoid glucose addiction in cancer cells

Project description:Cancer cells consume large amounts of glucose because of their specific metabolic pathway. However, cancer cells exist in tumor tissue where glucose is insufficient. To survive, cancer cells likely have the mechanism to elude their glucose addiction. Here we show that functional mitochondria are essential if cancer cells are to avoid glucose addiction. Cancer cells with dysfunctional mitochondria, such as mitochondrial DNA-deficient rho0 cells and electron transport chain blocker-treated cells, were highly sensitive to glucose deprivation. Our data demonstrated that this sensitization was caused by failure of the unfolded protein response (UPR), an adaptive response mediated by the endoplasmic reticulum (ER). This study suggests a link between mitochondria and the ER during the UPR under glucose deprivation conditions and that mitochondria govern cell fate, not only through ATP production and apoptosis regulation but also through modulating the UPR for cell survival. Human cancer cell lines (HT-1080, HT-29, and mtDNA-deficient cells derived from these cell lines) were selected for RNA extraction and hybridization on Affymetrix microarrays. We examined the unfolded protein response (UPR), an adaptive response mediated by the endoplasmic reticulum (ER), of cancer cells under stress conditions. Abbreviations List: AA, antimycin A; Bu, buformin; Met, metformin; Phen, phenformin; Rot, rotenone; VST, versipelostatin; TM, tunicamycin; 2DG, 2-deoxyglucose; GS, glucose starvation. Capital S (_S) indicates the supernatant of sample including floating cells.

2010-05-28 | E-GEOD-16157 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data