Expression Data from ALDH1+ breast cancer stem cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE83811 | GEO | 2016/12/31
SECONDARY ACCESSION(S): PRJNA327081
REPOSITORIES: GEO
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Project description:Cancer stem cells (CSCs) drive tumor growth, metastasis, relapse, and chemoresistance. However, it’s unclear how lipid metabolism, especially sphingolipids metabolism, regulates CSCs and chemoresistance. In this study, we developed spontaneous tumor models expressing a Sox9-GFP transgenic reporter and demonstrated that cancer cells expressing high levels of SOX9 functioned as CSCs in both primary tumors and metastases. Transcriptomics analyses uncovered that SOX9high CSCs upregulate ABCA12 lipid transporter. Functionally, downregulation of ABCA12 impaired cancer stemness and chemoresistance of SOX9high cells. Through lipidomic analysis, we demonstrated that ABCA12 regulates SOX9 expression and cancer stemness by controlling ceramide abundance. Blocking ceramide hydrolysis using acid ceramidase inhibitor D-NMAPPD sensitized tumors to chemotherapy and prevented enrichment of SOX9high CSCs. These data suggest a potential strategy for targeting CSCs and overcoming chemoresistance. We further demonstrated that ceramide inhibits the YAP/TAZ signaling that is required for SOX9 expression in breast CSCs.
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Project description:Cancer stem cells (CSCs) are proposed to be responsible for metastatic dissemination and clinical relapse in a variety of cancers. Analogies between CSCs and normal tissue stem cells (SC) has led to the notion that CSCs often co-opt the normal SC program of their tissue-of-origin. The cell-biological program termed epithelial-mesenchymal transition (EMT) has been found to encourage entrance of normal and neoplastic mammary cells into the corresponding SC states. Using genetically engineered knock-in reporter mouse lines, we demonstrate that in the murine mammary lineage, the paralogous EMT-inducing transcription factors Snail and Slug, are selectively exploited by CSCs and normal SCs respectively. Slug, when expressed at physiological levels, only activates a partial EMT program and is dispensable in CSCs. In contrast, Snail drives a far more complete transition into the mesenchymal state and controls both tumor-initiation and metastatic dissemination. Consistent with their functional distinctions, Snail controls far more target genes than Slug, and their distinct functions are determined by their divergent N-terminal domains. Our findings underscore fundamental distinctions between the SC program operating in normal and neoplastic SCs, and hint for potential avenues of selective therapeutic elimination of breast CSCs. We sought to understand differential ability to activate the EMT program in breast cancer cells by transcription factors Snail and Slug. Hence, we mapped genome-wide Snail and Slug binding sites in murine MMTV-PyMT breast cancer cell lines that express high level of Snail or high level of Slug respectively. Specifically, we performed Snail ChIP seq in the mesenchymal pBl.3G cells, and Slug ChIP-seq in the epithelial pBl.1G cells.
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Project description:Mufudza2012 - Estrogen effect on the dynamics
of breast cancer
This deterministic model shows the
dynamics of breast cancer with immune response. The effects of
estrogen are incorporated to study its effects as a risk factor for
the disease.
This model is described in the article:
Assessing the effects of
estrogen on the dynamics of breast cancer.
Mufudza C, Sorofa W, Chiyaka
ET.
Comput Math Methods Med 2012; 2012:
473572
Abstract:
Worldwide, breast cancer has become the second most common
cancer in women. The disease has currently been named the most
deadly cancer in women but little is known on what causes the
disease. We present the effects of estrogen as a risk factor on
the dynamics of breast cancer. We develop a deterministic
mathematical model showing general dynamics of breast cancer
with immune response. This is a four-population model that
includes tumor cells, host cells, immune cells, and estrogen.
The effects of estrogen are then incorporated in the model. The
results show that the presence of extra estrogen increases the
risk of developing breast cancer.
This model is hosted on
BioModels Database
and identified by:
BIOMD0000000642.
To cite BioModels Database, please use:
BioModels Database:
An enhanced, curated and annotated resource for published
quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
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