Annick Klein
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Data from Tenascin-C Promotes Tumor Cell Migration and Metastasis through Integrin α9β1–Mediated YAP Inhibition Open
Tenascin-C is an extracellular matrix molecule that drives progression of many types of human cancer, but the basis for its actions remains obscure. In this study, we describe a cell-autonomous signaling mechanism explaining how tenascin-C…
Data from Tenascin-C Promotes Tumor Cell Migration and Metastasis through Integrin α9β1–Mediated YAP Inhibition Open
Tenascin-C is an extracellular matrix molecule that drives progression of many types of human cancer, but the basis for its actions remains obscure. In this study, we describe a cell-autonomous signaling mechanism explaining how tenascin-C…
Supplementary data from Tenascin-C Promotes Tumor Cell Migration and Metastasis through Integrin α9β1–Mediated YAP Inhibition Open
Supplementary data
Video1.FN from Tenascin-C Promotes Tumor Cell Migration and Metastasis through Integrin α9β1–Mediated YAP Inhibition Open
KRIB cell migration on FN
Video2.FN.TNC from Tenascin-C Promotes Tumor Cell Migration and Metastasis through Integrin α9β1–Mediated YAP Inhibition Open
KRIB cell migration on FN/TNC
Video2.FN.TNC from Tenascin-C Promotes Tumor Cell Migration and Metastasis through Integrin α9β1–Mediated YAP Inhibition Open
KRIB cell migration on FN/TNC
Supplementary data from Tenascin-C Promotes Tumor Cell Migration and Metastasis through Integrin α9β1–Mediated YAP Inhibition Open
Supplementary data
Video1.FN from Tenascin-C Promotes Tumor Cell Migration and Metastasis through Integrin α9β1–Mediated YAP Inhibition Open
KRIB cell migration on FN
Ral GTPases promote breast cancer metastasis by controlling biogenesis and organ targeting of exosomes Open
Cancer extracellular vesicles (EVs) shuttle at distance and fertilize pre-metastatic niches facilitating subsequent seeding by tumor cells. However, the link between EV secretion mechanisms and their capacity to form pre-metastatic niches …
Author response: Ral GTPases promote breast cancer metastasis by controlling biogenesis and organ targeting of exosomes Open
Article Figures and data Abstract Introduction Results Discussion Materials and methods Data availability References Decision letter Author response Article and author information Metrics Abstract Cancer extracellular vesicles (EVs) shuttl…
Tenascin-C increases lung metastasis by impacting blood vessel invasions Open
Metastasis is a major cause of death in cancer patients. The extracellular matrix molecule tenascin-C is a known promoter of metastasis, however the underlying mechanisms are not well understood. To further analyze the impact of tenascin-C…
Laminin α1 orchestrates VEGFA functions in the ecosystem of colorectal carcinoma Open
Background Information Tumor stroma remodeling is a key feature of malignant tumors and can promote cancer progression. Laminins are major constituents of basement membranes that physically separate the epithelium from the underlying strom…
Tenascin-C Promotes Tumor Cell Migration and Metastasis through Integrin α9β1–Mediated YAP Inhibition Open
Tenascin-C is an extracellular matrix molecule that drives progression of many types of human cancer, but the basis for its actions remains obscure. In this study, we describe a cell-autonomous signaling mechanism explaining how tenascin-C…
Tenascin-C Orchestrates Glioblastoma Angiogenesis by Modulation of Pro- and Anti-angiogenic Signaling Open
High expression of the extracellular matrix component tenascin-C in the tumor microenvironment correlates with decreased patient survival. Tenascin-C promotes cancer progression and a disrupted tumor vasculature through an unclear mechanis…