Cell-ECM Interactions in Tumor Invasion

He, Xiuxiu; Lee, Byoungkoo; Jiang, Yi

doi:10.1007/978-3-319-42023-3_4

Cited by 70 publications

(53 citation statements)

References 113 publications

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“…Importantly, inflammatory cytokines can disrupt TJ complexes by decreasing the expression of TJ molecules, including TJP1, which is consistent with our observations in UM [ 25 ]. Additionally, the importance of cell–ECM interactions, especially with FAs, in regulating and contributing to cancer migration and invasion has been increasingly accepted [ 26 ]. As the critical components of FA structures, both ECM molecules (FN1 and ICAM-1) and cell-surface receptors (integrin subunits) were induced by IL-6 in UM cells.…”

Section: Discussionmentioning

confidence: 99%

Abnormally expressed JunB transactivated by IL-6/STAT3 signaling promotes uveal melanoma aggressiveness via epithelial–mesenchymal transition

Gong

Shen

Fang³

et al. 2018

Bioscience Reports

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Uveal melanoma (UM) is the most common primary intraocular tumor in adults, and it carries a high risk of metastasis and mortality. Various proinflammatory cytokines have been found to be significantly increased in the aqueous humor or vitreous fluid of UM patients; however, the role of these cytokines in UM metastasis remains elusive. In the present study, we found that long-term interleukin (IL)-6 exposure promoted the migration and invasion of UM cells, diminished cell–cell adhesion, and enhanced focal adhesion. Moreover, IL-6 treatment decreased the membranous epithelial marker TJP1 and increased the cytoplasmic mesenchymal marker Vimentin. Further investigation demonstrated that JunB played a critical role in IL-6-induced UM epithelial–mesenchymal transition (EMT). In UM cells, the expression of JunB was significantly up-regulated during the IL-6-driven EMT process. Additionally, JunB induction occurred at the transcriptional level in a manner dependent on phosphorylated STAT3, during which activated STAT3 directly bound to the JunB promoter. Importantly, the knockdown of STAT3 prevented the IL-6-induced EMT phenotype as well as cell migration and invasion, whereas JunB overexpression recovered the attenuated aggressiveness of UM cells. Similarly, with IL-6 stimulation, the stable overexpression of JunB strengthened the migratory and invasive capabilities of UM cells and induced the EMT-promoting factors (Snail, Twist1, matrix metalloproteinase (MMP)-2, MMP-14, and MMP-19). Analysis of The Cancer Genome Atlas (TCGA) database indicated that JunB was positively correlated with IL-6 and STAT3 in UM tissues. The present study proposes an IL-6/STAT3/JunB axis leading to UM aggressiveness by EMT, which illustrates the negative side of inflammatory response in UM metastasis.

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Section: Discussionmentioning

confidence: 99%

Abnormally expressed JunB transactivated by IL-6/STAT3 signaling promotes uveal melanoma aggressiveness via epithelial–mesenchymal transition

Gong

Shen

Fang³

et al. 2018

Bioscience Reports

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“…Cadherins, integrins, selectins, and members of the immunoglobulin superfamily are the four major groups of CAMs mainly involved in transduction signaling, cytoskeletal organization, and gene regulation upon cell-to-cell and cell-to-ECM interactions [38,39]. Hence, alterations in their expression may contribute to peculiar features of neoplastic transformation, including the loss of cellular morphology and tissue architecture [40,41] as well as cell invasion, migration, EMT, trans-endothelial migration, intra-and extra-vasation, tumor angiogenesis, and organ-specific metastasis [42]. In line with our and other previous studies [12,43,44], the present data analysis determined that one of the most GPER-correlated genes belonging to the CAMs pathway is the microvessel density marker CD34.…”

Section: Discussionmentioning

confidence: 99%

The G Protein-Coupled Estrogen Receptor (GPER) Expression Correlates with Pro-Metastatic Pathways in ER-Negative Breast Cancer: A Bioinformatics Analysis

Talia

Francesco

Rigiracciolo

et al. 2020

Cells

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The G protein-coupled estrogen receptor (GPER, formerly known as GPR30) is a seven-transmembrane receptor that mediates estrogen signals in both normal and malignant cells. In particular, GPER has been involved in the activation of diverse signaling pathways toward transcriptional and biological responses that characterize the progression of breast cancer (BC). In this context, a correlation between GPER expression and worse clinical-pathological features of BC has been suggested, although controversial data have also been reported. In order to better assess the biological significance of GPER in the aggressive estrogen receptor (ER)-negative BC, we performed a bioinformatics analysis using the information provided by The Invasive Breast Cancer Cohort of The Cancer Genome Atlas (TCGA) project and Molecular Taxonomy of Breast Cancer International Consortium (METABRIC) datasets. Gene expression correlation and the statistical analysis were carried out with R studio base functions and the tidyverse package. Pathway enrichment analysis was evaluated with Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway on the Database for Annotation, Visualization and Integrated Discovery (DAVID) website, whereas gene set enrichment analysis (GSEA) was performed with the R package phenoTest. The survival analysis was determined with the R package survivALL. Analyzing the expression data of more than 2500 primary BC, we ascertained that GPER levels are associated with pro-migratory and metastatic genes belonging to cell adhesion molecules (CAMs), extracellular matrix (ECM)-receptor interaction, and focal adhesion (FA) signaling pathways. Thereafter, evaluating the disease-free interval (DFI) in ER-negative BC patients, we found that the subjects expressing high GPER levels exhibited a shorter DFI in respect to those exhibiting low GPER levels. Overall, our results may pave the way to further dissect the network triggered by GPER in the breast malignancies lacking ER toward a better assessment of its prognostic significance and the action elicited in mediating the aggressive features of the aforementioned BC subtype.

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“…Collagens account for~30% of body proteins and are a major part of the ECM (extracellular matrix) [53][54][55][56]. Collagen from ECM is known to regulate multiple signaling pathways that control cancer cell behavior by regulating mortality and invasiveness of cells [10,[57][58][59]. In tumor micro environmental ECM, type I collagen exhibit in high density and are known to be associated with tumor aggressiveness [60][61][62][63].…”

Section: Ddr1 In Tumor Progression and Metastasismentioning

confidence: 99%

Signaling by discoidin domain receptor 1 in cancer metastasis

Gadiya

Chakraborty

2018

Cell Adhesion & Migration

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Collagen is the most abundant component of tumor extracellular matrix (ECM). ECM collagens are known to directly interact with the tumor cells via cell surface receptor and play crucial role in tumor cell survival and promote tumor progression. Collagen receptor DDR1 is a member of receptor tyrosine kinase (RTK) family with a unique motif in the extracellular domain resembling Dictyostelium discoideum protein discoidin-I. DDR1 displays delayed and sustained activation upon interaction with collagen and recent findings have demonstrated that DDR1-collagen signaling play important role in cancer progression. In this review, we discuss the current knowledge on the role of DDR1 in cancer metastasis and possibility of a potential therapeutic approach of DDR1 targeted therapy in cancer.

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Cell-ECM Interactions in Tumor Invasion

Cited by 70 publications

References 113 publications

Abnormally expressed JunB transactivated by IL-6/STAT3 signaling promotes uveal melanoma aggressiveness via epithelial–mesenchymal transition

Abnormally expressed JunB transactivated by IL-6/STAT3 signaling promotes uveal melanoma aggressiveness via epithelial–mesenchymal transition

The G Protein-Coupled Estrogen Receptor (GPER) Expression Correlates with Pro-Metastatic Pathways in ER-Negative Breast Cancer: A Bioinformatics Analysis

Signaling by discoidin domain receptor 1 in cancer metastasis

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