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TGF-β signaling activated by cancer-associated fibroblasts determines the histological signature of lung adenocarcinoma

ABSTRACT: TGF-β signaling activated by cancer-associated fibroblasts determines the histological signature of lung adenocarcinoma

PROVIDER: PRJNA714926 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13979021.fastq.gz	Fastqsanger.gz
	SRR13979022.fastq.gz	Fastqsanger.gz
	SRR13979023.fastq.gz	Fastqsanger.gz
	SRR13979024.fastq.gz	Fastqsanger.gz

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TGF-β signaling activated by cancer-associated fibroblasts determines the histological signature of lung adenocarcinoma

Project description:Invasive lung adenocarcinoma (LADC) is classified histologically as lepidic, acinar, papillary, micropapillary, or solid. We found that A549 human LADC cells formed tumors with distinct histological features—solid-type or acinar-type tumors—depending on the site of development in immunodeficient mice and that a solid-to-acinar transition (SAT) could be induced by cancer-associated fibroblasts (CAFs) in 3D cocultures with A549. To clarify the molecular mechanisms contributing to SAT induction, we performed RNA-seq analysis of four A549 tumor cell samples derived from solid- or acinar-type tumor tissue formed in vivo or from 3D tumor colonies formed in the presence or absence of CAFs in vitro.

2022-03-15 | GSE169029 | GEO

TGFβ Signaling Activated by Cancer-Associated Fibroblasts Determines the Histological Signature of Lung Adenocarcinoma.

Project description:Invasive lung adenocarcinoma (LADC) can be classified histologically as lepidic, acinar, papillary, micropapillary, or solid. Most LADC tumors manifest several of these histological subtypes, with heterogeneity being related to therapeutic resistance. We report here that in immunodeficient mice, human LADC cells form tumors with distinct histological features, MUC5AC-expressing solid-type or cytokeratin 7 (CK7)-expressing acinar-type tumors, depending on the site of development, and that a solid-to-acinar transition (SAT) could be induced by the tumor microenvironment. The TGFβ-Smad signaling pathway was activated in both tumor and stromal cells of acinar-type tumors. Immortalized cancer-associated fibroblasts (CAF) derived from acinar-type tumors induced SAT in 3D cocultures with LADC cells. Exogenous TGFβ1 or overexpression of an active form of TGFβ1 increased CK7 expression and reduced MUC5AC expression in LADC cells, and knockdown of Tgfb1 mRNA in CAFs attenuated SAT induction. RNA-sequencing analysis suggested that angiogenesis and neutrophil recruitment are associated with SAT in vivo. Our data indicate that CAF-mediated paracrine TGFβ signaling induces remodeling of tumor tissue and determines the histological pattern of LADC, thereby contributing to tumor heterogeneity. SIGNIFICANCE: CAFs secrete TGFβ to induce a solid-to-acinar transition in lung cancer cells, demonstrating how the tumor microenvironment influences histological patterns and tumor heterogeneity in lung adenocarcinoma.

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Project description:TGF-beta treatment of Panc-1 pancreatic adenocarcinoma cell line on Affymetrix HG_U133_plus_2 arrays; triplicate experiments. The goal of the experiment is to profile temporal gene expression changes during TGF-beta-induced epithelial-mesenchymal transition (EMT). During EMT cancer cells lose their epithelial specifc proteins and gain mesenchymal proteins to acquire migratory and invasive phenotype essential for metastasis. Human Panc-1 pancreatic adenocarcinoma cell line was treated with 5 ng/mL TGF-beta for 48 h to induce EMT. The experiment was repeated 3 times. Samples were assayed using Affymetrix HG_U133_plus_2 arrays with 54675 probe-sets, using standard techniques. Human Panc-1 pancreatic adenocarcinoma cell line was treated with 5 ng/mL TGF-beta for 48 h. The experiment was repeated 3 times. Samples were assayed using Affymetrix HG_U133_plus_2 arrays with 54675 probe-sets, using standard techniques.

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Project description:Association of frequent hypermethylation with high grade histological subtype in lung adenocarcinoma. (Infinium Methylation450K)

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