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IGFBP3 Promotes Mammary Stem Cells Activity and Tumorigenesis by Regulating IGF Bioavailability

ABSTRACT: IGFBP3 Promotes Mammary Stem Cells Activity and Tumorigenesis by Regulating IGF Bioavailability

PROVIDER: PRJNA1227909 | ENA |

REPOSITORIES: ENA

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IGFBP3 Promotes Mammary Stem Cells Activity and Tumorigenesis by Regulating IGF Bioavailability

Project description:Mammary stem cells (MaSCs) play important roles in mammary gland homeostasis. A better understanding of MaSC activity enhances our knowledge of breast cancer initiation and progression, particularly in the context of triple-negative breast cancer (TNBC). Until now, the molecular mechanisms of MaSCs have remained elusive. Our current research has unveiled a significant enrichment of IGFBP3 expression in normal MaSCs, highlighting its indispensable role in maintaining MaSCs stemness and mammary gland development. Moreover, we show that IGFBP3 promotes breast cancer tumorigenesis and progression. Mechanistically, IGFBP3 regulates IGF1/2 bioavailability under the action of MMPs (such as MMP3), activating the IGF1R receptor and its downstream AKT and ERK1/2 signaling pathways. In clinical samples, high expression of either IGFBP3 or MMP3 is associated with poor prognosis in ER-negative or TNBC patients. Future studies should investigate the potential therapeutic benefit of IGFBP3 in TNBC.

2025-07-01 | GSE290400 | GEO

Mammary Tissue: Wild type mammary glands vs IGF-IR induced mammary tumors vs IGF-IR independent tumors

Project description:Molecular profiling was used to classify mammary tumors that develop in MTB-IGFIR transgenic mice. It was determined that the primary mammary tumors (PMT), which develop due to elevated expression of the type I insulin-like growth factor receptor (IGF-IR) in mammary epithelial cells, most closely resemble murine tumors with basal-like or mixed gene expression profiles and with human basal-like breast cancers. Downregulation of IGF-IR transgene in MTB-IGFIR tumor-bearing mice leads to the regression of most of the tumors followed by tumor re-appearance in some of the mice. These tumors that re-appear following IGF-IR transgene downregulation do not express the IGF-IR transgene and cluster with murine mammary tumors that express a mesenchymal gene expression profile and with human claudin-low breast cancers. Therefore, IGF-IR overexpression in murine mammary epithelial cells induces mammary tumors with primarily basal-like characteristics while tumors that develop following IGF-IR downregulation express a gene signature that most closely resembles human claudin-low breast tumors.

2011-10-01 | GSE32152 | GEO

Mammary Tissue: Wild type mammary glands vs IGF-IR induced mammary tumors vs IGF-IR independent tumors

2011-09-30 | E-GEOD-32152 | biostudies-arrayexpress

Overexpression of IGF-1 During Early Development Expands the Number of Mammary Stem Cells and Primes them for Transformation

Project description:In this paper we report transcriptomic profiles of mammary stem cells (MaSCs) from female BK5.IGF1 transgenic and age-matched WT mice, generated by single-cell RNA-sequencing technology. We found that IGF-1 stimulated quiescent MaSCs to enter the cell cycle and increased their expression of genes involved in proliferation, plasiticity, tumorigenesis, invasion, and metastasis.

2021-07-01 | GSE173988 | GEO

Mammary Tissue: aCGH of primary (IGF-IR induced) and recurrent (IGF-IR independent) mammary tumors from MTB-IGFIR mice

Project description:Mammary Tissue: aCGH of primary (IGF-IR induced) and recurrent (IGF-IR independent) mammary tumors from MTB-IGFIR mice

| PRJNA491906 | ENA

Rank pathway activation attenuates mammary tumorigenesis by inducing senescence

Project description:Rank overexpression attenuates mammary tumorigenesis by inducing senescence in mammary epithelial cells but enhances tumor aggressiveness by increasing stemness.

2022-02-24 | GSE139675 | GEO

Insulin Receptor Loss Impairs Mammary Tumorigenesis in Mice

Project description:Insulin Receptor Loss Impairs Mammary Tumorigenesis in Mice

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EMT inducers catalyze malignant transformation of mammary epithelial cells and drive tumorigenesis towards claudin-low tumors

Project description:This SuperSeries is composed of the following subset Series: GSE32727: EMT inducers catalyze malignant transformation of mammary epithelial cells and drive tumorigenesis towards claudin-low tumors [human] GSE32904: EMT inducers catalyze malignant transformation of mammary epithelial cells and drive tumorigenesis towards claudin-low tumors [mouse] Refer to individual Series

2012-07-23 | E-GEOD-32905 | biostudies-arrayexpress

Regulation of mammary luminal cell differentiation and tumorigenesis by p38α

Project description:Mammary stem and progenitor cells are essential for mammary gland homeostasis and are also candidates for cells of origin of mammary tumors. Here, we provide evidence that the protein kinase p38a is required for the differentiation of luminal progenitor cells through modulation of the transcription factors Runx1 and Foxa1. Moreover, using a mouse model for breast cancer initiated by luminal cells, we show that p38a downregulation in mammary epithelial cells reduces tumorigenesis, which correlates with reduced numbers of tumor-initiating cells. Our results identify p38a as a key regulator of luminal progenitor cell fate that facilitates mammary tumor formation.

2017-12-28 | GSE92877 | GEO

Gene expression of spheres made from mammary tumors of FRS2b hetero mice and knock-out mice

Project description:Precancerous tissue microenvironment is thought to be important for tumorigenesis when cancer stem-like cells (CSCs) begin to grow, though underlying mechanisms remain unclear. Here, we uncovered critical roles of luminal progenitor cells expressing FRS2β, an inhibitory adaptor for ErbB signaling, to create the cytokines-rich CSC niche in mammary tissues. Deficiency of FRS2β greatly decreased mammary tumorigenesis with decreased tumor stroma in mouse mammary tumor virus (MMTV)-ErbB2 mice. Moreover, FRS2β-deficient precancerous mammary tissues did not allow tumorigenesis derived from xenografted wild type FRS2β tumor cells. Insulin-like growth factor (IGF) 1 and CXC chemokine ligand (CXCL) 12, stemness- and stroma-inducing cytokines, respectively, were expressed at low levels in FRS2β-deficient precancerous mammary cells. Treatment with inhibitors against these cytokines in precancerous mice greatly decreased tumorigenic potential. In addition, human breast cancer tissues in which FRS2β is highly expressed in tumor cells harbor more stroma, and are associated with poor prognosis. Thus, cytokines-rich CSC niche and tumor microenvironment induced by FRS2β expressed in luminal progenitor cells and tumor cells play important roles for tumorigenesis.

2021-09-07 | GSE120034 | GEO

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