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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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IL-17 mediates susceptibility to breast cancer growth by promoting the recruitment of tumorigenic neutrophils

ABSTRACT: The aggressiveness of invasive ductal carcinoma (IDC) of the breast is associated with increased IL-17 levels. In this study, we investigated the role of IL-17 in invasive breast tumor pathogenesis. We found that metastatic tumor-infiltrating T lymphocytes produced elevated levels of IL-17, whereas IL-17 neutralization inhibited tumor growth and prevented the migration of neutrophils and tumor cells to secondary disease sites. Tumorigenic neutrophils promote disease progression, and their depletion suppressed tumor growth. Moreover, IL-17 induced IL-6 and CXCL1 production in tumor cells, and IL-6 depletion reduced metastatic tumor growth and infiltration by Th17 cells and neutrophils. In addition, inoculation of a non-metastatic mammary tumor cell line pre-incubated with IL-17 promoted tumor growth, confirming the pro-tumor role of IL-17. Furthermore, high IL-17 expression was associated with lower disease-free survival (DFS) and worse prognosis in IDC patients. Thus, IL-17 blockade represents an attractive approach for the control of invasive breast tumors. Biopsies of patients with breast tumors

ORGANISM(S): Homo sapiens

SUBMITTER: Daniel De Carvalho

PROVIDER: E-GEOD-56822 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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IL-17 mediates susceptibility to breast cancer growth by promoting the recruitment of tumorigenic neutrophils

Project description:The aggressiveness of invasive ductal carcinoma (IDC) of the breast is associated with increased IL-17 levels. In this study, we investigated the role of IL-17 in invasive breast tumor pathogenesis. We found that metastatic tumor-infiltrating T lymphocytes produced elevated levels of IL-17, whereas IL-17 neutralization inhibited tumor growth and prevented the migration of neutrophils and tumor cells to secondary disease sites. Tumorigenic neutrophils promote disease progression, and their depletion suppressed tumor growth. Moreover, IL-17 induced IL-6 and CXCL1 production in tumor cells, and IL-6 depletion reduced metastatic tumor growth and infiltration by Th17 cells and neutrophils. In addition, inoculation of a non-metastatic mammary tumor cell line pre-incubated with IL-17 promoted tumor growth, confirming the pro-tumor role of IL-17. Furthermore, high IL-17 expression was associated with lower disease-free survival (DFS) and worse prognosis in IDC patients. Thus, IL-17 blockade represents an attractive approach for the control of invasive breast tumors.

2015-04-01 | GSE56822 | GEO

cDNA aCGH study of pure DCIS without invasive tumor, DCIS associated with IDC and its IDC component

Project description:cDNA aCGH study of pure DCIS (breast duct carcinoma in situ) without invasive tumor, DCIS associated with IDC (breast invasive duct carcinoma) and its IDC component 23 patients: 6 pure DCIS without invasive cancer and no history of invasive cancer, 17 DCIS associated with IDC. Out of the latter 1 tumor had only enough DCIS (#16) for aCGH and one - IDC (#23) Keywords: Comparative clinical study

2009-02-01 | GSE10197 | GEO

Transcriptome analysis reveals differences in cell cycle, growth and migration related genes that distinguish fibroblasts derived from pre-invasive and invasive breast cancer.

Project description:As the most common form of pre-invasive breast cancer, ductal carcinoma in situ (DCIS) affects over 50,000 women in the US annually. Despite standardized treatment involving lumpectomy and radiation therapy, up to 25 % of patients with DCIS experience disease recurrence often with invasive ductal carcinoma (IDC), indicating that a subset of patients may be under-treated. As most DCIS cases will not progress to invasion, many patients may experience over-treatment. By understanding the underlying processes associated with DCIS to IDC progression, we can identify new biomarkers to determine which DCIS cases may become invasive and improve treatment for patients. Accumulation of fibroblasts in IDC is associated with disease progression and reduced survival. While fibroblasts have been detected in DCIS, little is understood about their role in DCIS progression.We sought to determine whether DCIS fibroblasts were similar or distinct from normal and IDC fibroblasts at the transcriptome level, fibroblasts underwent transcriptome profilingthrough bulk RNA seq and pathway analysis. DCIS fibroblasts are phenotypically distinct from normal breast and IDC fibroblasts, and play an important role in breast cancer growth, invasion, and recruitment of myeloid cells. These studies provide novel insight into the role of DCIS fibroblasts in breast cancer progression and identify some key biomarkers associated with DCIS progression to IDC, with important clinical implications.

2023-03-31 | GSE228582 | GEO

Immune landscape in ER+ breast cancer subtypes identifies a differential role for macrophages

Project description:Current immunotherapies are ineffective for estrogen receptor positive (ER+) breast cancers, which account for nearly 70% of all breast cancers. Amongst the ER+ breast cancers, the major subtypes are invasive ductal carcinoma (IDC) and invasive lobular carcinoma (ILC). We utilized droplet-based single-cell RNAseq (10X Genomics) to analyzed the immune landscape of both peripheral blood and tumor infiltrating immune populations in both IDC and ILC. These analyses demonstrated substantial heterogeneity of macrophage within the tumor microenvironment.

2023-01-29 | GSE193911 | GEO

Expression data from breast tumors in different age-specific cohorts and for different sequentional disease stages

Project description:Compared transccriptome of breast cancer in young women to those arising in two mature groups to characterize the underlying biological mechanisms of the breast cancer in Middle Eastern young women. Also, compared the gene expression profile characteristic of the sequential disease stages (ductal carcinoma in situ (DCIS) and invasive ductal carcinoma (IDC)) of breast cancer to elucidate the molecular mechanisms of breast cancer progression in young women. Analyzed the whole-genome mRNA expression profile from tumor (n=73) and adjacent disease free tissues (n=36) using Affymetrix GeneChip Human Genome U133 Plus 2.0 Arrays.

2014-08-01 | E-GEOD-29044 | biostudies-arrayexpress

Glucocorticoid Receptor Activation in Lobular Breast Cancer is Associated with Reduced Cell Proliferation and Promotion of Metastases; SUM44-GR-GFP

Project description:Estrogen receptor-positive (ER+) invasive lobular breast cancer (ILC) comprises about ~15% of breast cancer. ILC’s unique genotypic (loss of wild type E-cadherin expression) and phenotypic (small individual round cancer cells that grow in discontinuous nests) are thought to contribute to a distinctive pattern of metastases to serosal membranes. Unlike invasive ductal carcinoma (IDC), ILC metastases often intercalate into the mesothelial layer of the peritoneum and other serosal surfaces. While ER activity is a known driver of ILC proliferation, very little is known about how additional nuclear receptors contribute to ILC’s distinctive biology. In ER+ IDC, we showed previously that glucocorticoid receptor (GR) activity inhibits pro-proliferative gene expression and cell proliferation. Here we examined ER+ ILC models and find that GR activation similarly reduces S-phase entry gene expression and ILC proliferation. While slowing tumor growth rate, our data also suggest that GR activation results in an enhanced metastatic phenotype through increasing integrin-encoding gene expression, extracellular matrix protein adhesion, and mesothelial cell clearance. Moreover, in an intraductal mouse mammary gland model of ILC, we found that GR expression is associated with increased metastases despite slowed primary mammary tumor growth. Taken together, our findings suggest GR-mediated gene expression may contribute to the unusual characteristics of ILC biology.

2023-09-04 | GSE241992 | GEO

Glucocorticoid Receptor Activation in Lobular Breast Cancer is Associated with Reduced Cell Proliferation and Promotion of Metastases; MM134

2023-09-04 | GSE241993 | GEO

RNA-Seq of ILC and IDC breast cancer cell lines in attached (2D) and suspension (ultra-low attachment) cultures

Project description:Invasive lobular carcinoma (ILC) is a histological subtype of breast cancer with distinct molecular and clinical features from the more common subtype invasive ductal carcinoma (IDC). ILC cells exhibit anchorage-independent growth in ultra-low attachment (ULA) suspension cultures, which is largely attributed to the loss of E-cadherin. In addition to anoikis resistance, herein we show that human ILC cell lines exhibit enhanced cell proliferation in ULA cultures as compared to IDC cells. Proteomic comparison of ILC and IDC cell lines identified induction of PI3K/Akt and p90-RSK pathways specifically in ULA culture in ILC cells. Further transcriptional profiling uncovered unique upregulation of the inhibitors of differentiation family transcription factors ID1 and ID3 in ILC ULA culture, the knockdown of which diminished the anchorage-independent growth of ILC cell lines through cell cycle arrest. We find that ID1 and ID3 expression is higher in human ILC tumors as compared to IDC, correlated with worse prognosis uniquely in patients with ILC and associated with upregulation of angiogenesis and matrisome-related genes. Altogether, our comprehensive study of anchorage independence in human ILC cell lines provides mechanistic insights and clinical implications for metastatic dissemination of ILC and implicates ID1 and ID3 as novel drivers and therapeutic targets for lobular breast cancer.

2020-06-23 | GSE130650 | GEO

The induction of an epithelial gene program promotes traits of mammary progenitor luminal cells

Project description:MicroRNAs are critical regulators of gene networks in normal and abnormal biological processes. Focusing on invasive ductal breast cancer (IDC), we have found dysregulated expression in tumor samples of several microRNAs, including the miR-200 family, along progression from primary tumors to distant metastases, further reflected in higher blood levels of miR-200b and miR-7 in IDC patients with regional or distant metastases relative to patients with primary node-negative tumors. Forced expression of miR-200s in MCF10CA1h mammary cells induced an enhanced epithelial program, aldehyde dehydrogenase (ALDH) activity, mammosphere growth and ability to form branched tubuloalveolar structures while promoting orthotopic tumor growth and lung colonization in vivo. Knockdown of the miR-200 target, ZEB2, partially phenocopied the expression of miR200s with a strong enhancement of mammosphere growth and ALDH activity. Interestingly, the morphology of tumors formed in vivo by cells expressing miR-200s was reminiscent of metaplastic breast cancer (MBC). Indeed, the epithelial components of MBC samples expressed significantly higher levels of miR-200s than their mesenchymal components and displayed a marker profile compatible with luminal progenitor cells. We propose that microRNAs of the miR-200 family promote traits of highly proliferative breast luminal progenitor cells, thereby exacerbating the growth and metastatic properties of transformed mammary epithelial cells.

2017-05-01 | GSE86995 | GEO

An Engineered Niche Delineates Metastatic Potential of Breast Cancer

Project description:We aimed to identify metastatic disease prior to the formation of an overt secondary tumor in triple-negative breast cancer using sister cell lines 4T1 (metastatic), 4T07 (invasive, non-metastatic), and 67NR (non-metastatic). We used a porous, polycaprolactone scaffold, that serves as an engineered metastatic niche, to identify metastatic disease through the changing microenvironment.

2023-11-06 | GSE233001 | GEO

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