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Transcription profiling by array of human primary pancreatic cancer cells and cancer associated fibroblasts co-cultured to study the cross talk between these cells

ABSTRACT: Coculture of primary pancreatic cancer cells and cancer associated fibroblasts (CAF) in vitro to study the cross talk between these cells

ORGANISM(S): Homo sapiens

SUBMITTER: Larsson Marie

PROVIDER: S-ECPF-MEXP-2826 | biostudies-other |

REPOSITORIES: biostudies-other

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Transcription profiling by array of human primary pancreatic cancer cells and cancer associated fibroblasts co-cultured to study the cross talk between these cells

Project description:Coculture of primary pancreatic cancer cells and cancer associated fibroblasts (CAF) in vitro to study the cross talk between these cells

2010-12-31 | E-MEXP-2826 | biostudies-arrayexpress

CCL2 mediates cross-talk between cancer cells and stromal fibroblasts that regulates breast cancer stem cells.

Project description:Cancer stem cells (CSC) play critical roles in cancer initiation, progression, and therapeutic refractoriness. Although many studies have focused on the genes and pathways involved in stemness, characterization of the factors in the tumor microenvironment that regulate CSCs is lacking. In this study, we investigated the effects of stromal fibroblasts on breast cancer stem cells. We found that compared with normal fibroblasts, primary cancer-associated fibroblasts (CAF) and fibroblasts activated by cocultured breast cancer cells produce higher levels of chemokine (C-C motif) ligand 2 (CCL2), which stimulates the stem cell-specific, sphere-forming phenotype in breast cancer cells and CSC self-renewal. Increased CCL2 expression in activated fibroblasts required STAT3 activation by diverse breast cancer-secreted cytokines, and in turn, induced NOTCH1 expression and the CSC features in breast cancer cells, constituting a cancer-stroma-cancer signaling circuit. In a xenograft model of paired fibroblasts and breast cancer tumor cells, loss of CCL2 significantly inhibited tumorigenesis and NOTCH1 expression. In addition, upregulation of both NOTCH1 and CCL2 was associated with poor differentiation in primary breast cancers, further supporting the observation that NOTCH1 is regulated by CCL2. Our findings therefore suggest that CCL2 represents a potential therapeutic target that can block the cancer-host communication that prompts CSC-mediated disease progression.

| S-EPMC3367125 | biostudies-literature

Gene expression of human cancer cells co-cultured with mouse astrocytes and fibroblasts after series of cross co-culture

Project description:Brain metastases are highly resistant to chemotherapy. Brain metastases are surrounded and infiltrated by activated astrocytes. To examine the genes whose expression is associated with chemo-resistance of brain-metastasized cancer cells, gene expression data were collected and analyzed from breast cancer cells and lung cancer cells co-cultured with astrocytes. Fibroblast cells were used as control. Human lung cancer cell PC14 was co-cultured with mouse astrocytes or fibroblasts for two rounds. Total RNAs were extracted from co-cultured cells and hybridized to human microarray.

| S-ECPF-GEOD-26292 | biostudies-other

Cross species hybridization of human cancer cells co-cultured with mouse astrocytes and fibroblasts (Illumina mouse-6)

Project description:Brain metastases are highly resistant to chemotherapy. Brain metastases are surrounded and infiltrated by activated astrocytes. To examine the genes whose expression is associated with chemo-resistance of brain-metastasized cancer cells, gene expression data were collected and analyzed from breast cancer cells and lung cancer cells co-cultured with astrocytes. Fibroblast cells were used as control. Total RNAs were extracted from co-cultured cells and hybridized to human microarray and mouse microarrays to detect human cell and mouse cell specific gene expression data.

| S-ECPF-GEOD-26261 | biostudies-other

Cross species hybridization of human cancer cells co-cultured with mouse astrocytes and fibroblasts (Illumina human-6)

Project description:Brain metastases are highly resistant to chemotherapy. Brain metastases are surrounded and infiltrated by activated astrocytes. To examine the genes whose expression is associated with chemo-resistance of brain-metastasized cancer cells, gene expression data were collected and analyzed from breast cancer cells and lung cancer cells co-cultured with astrocytes. Fibroblast cells were used as control. Total RNAs were extracted from co-cultured cells and hybridized to human microarray and mouse microarrays to detect human cell and mouse cell specific gene expression data.

| S-ECPF-GEOD-26291 | biostudies-other

Cross species hybridization of human cancer cells co-cultured with mouse astrocytes and fibroblasts

Project description:This SuperSeries is composed of the SubSeries listed below.

2012-12-31 | GSE26293 | GEO

Cross species hybridization of human cancer cells co-cultured with mouse astrocytes and fibroblasts

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2012-12-31 | E-GEOD-26293 | biostudies-arrayexpress

Targeting cancer-associated fibroblasts/tumor cells cross-talk inhibits intrahepatic cholangiocarcinoma progression via cell-cycle arrest.

Project description:BackgroundCancer-associated fibroblasts (CAFs), mainly responsible for the desmoplastic reaction hallmark of intrahepatic Cholangiocarcinoma (iCCA), likely have a role in tumor aggressiveness and resistance to therapy, although the molecular mechanisms involved are unknown. Aim of the study is to investigate how targeting hCAF/iCCA cross-talk with a Notch1 inhibitor, namely Crenigacestat, may affect cancer progression.MethodsWe used different in vitro models in 2D and established new 3D hetero-spheroids with iCCA cells and human (h)CAFs. The results were confirmed in a xenograft model, and explanted tumoral tissues underwent transcriptomic and bioinformatic analysis.ResultshCAFs/iCCA cross-talk sustains increased migration of both KKU-M213 and KKU-M156 cells, while Crenigacestat significantly inhibits only the cross-talk stimulated migration. Hetero-spheroids grew larger than homo-spheroids, formed by only iCCA cells. Crenigacestat significantly reduced the invasion and growth of hetero- but not of homo-spheroids. In xenograft models, hCAFs/KKU-M213 tumors grew significantly larger than KKU-M213 tumors, but were significantly reduced in volume by Crenigacestat treatment, which also significantly decreased the fibrotic reaction. Ingenuity pathway analysis revealed that genes of hCAFs/KKU-M213 but not of KKU-M213 tumors increased tumor lesions, and that Crenigacestat treatment inhibited the modulated canonical pathways. Cell cycle checkpoints were the most notably modulated pathway and Crenigacestat reduced CCNE2 gene expression, consequently inducing cell cycle arrest. In hetero-spheroids, the number of cells increased in the G2/M cell cycle phase, while Crenigacestat significantly decreased cell numbers in the G2/M phase in hetero but not in homo-spheroids.ConclusionsThe hCAFs/iCCA cross-talk is a new target for reducing cancer progression with drugs such as Crenigacestat.

| S-EPMC11484308 | biostudies-literature

Transcription profiling of human MCF10A cells co-cultured with breast fibroblasts from breast cancer tissues or normal breast tissues

Project description:The epigenetic influence from microenvironment on mammary epethelial cells was investigated by coculture MCF10A cells with different breast fibroblasts that extracted from either breast cancer tissues or normal breast tissues. Experiment Overall Design: MCF10A cells were cocultured with different breast fibroblasts that extracted from either breast cancer tissues or normal breast tissues. After three weeks coculture, MCF10A cells were sorted and harvested for total RNA extraction. Affymetrix expression microarray was performed to analyse gene expression changes.

| S-ECPF-GEOD-10046 | biostudies-other

Extracellular Vesicle-Dependent Cross-Talk in Cancer-Focus on Pancreatic Cancer.

Project description:Extracellular vesicles (EVs) like exosomes and shed microvesicles are generated by many different cells. However, among all the cells, cancer cells are now recognized to secrete more EVs than healthy cells. Tumor-derived EVs can be isolated from biofluids such as blood, urine, ascitic fluid, and saliva. Their numerous components (nucleic acids, proteins, and lipids) possess many pleiotropic functions involved in cancer progression. The tumor-derived EVs generated under the influence of tumor microenvironment play distant roles and promote cellular communication by directly interacting with different cells. Moreover, they modulate extracellular matrix remodeling and tumor progression. Tumor-derived EVs are involved in pre-metastatic niche formation, dependent on the EV-associated protein receptors, and in cancer chemoresistance as they transfer drug-resistance-related genes to recipient cells. Recent advances in preclinical and clinical fields suggest their potential use as biomarkers for diagnosis and prognosis as well as for drug delivery in cancer. In this Review, we discuss EV characteristics and pro-tumor capacities, and highlight the future crucial impact of tumor-derived EVs in pancreatic cancer diagnosis and prognosis.

| S-EPMC7466446 | biostudies-literature

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