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Fig. 2 | Journal of Experimental & Clinical Cancer Research

Fig. 2

From: Exploring the interaction between extracellular matrix components in a 3D organoid disease model to replicate the pathophysiology of breast cancer

Fig. 2

Schematic representation of the role of collagen and Fibronectin as ECM components and integrin-mediated downstream signaling 1) ILK prevents the activity of myosin phosphatase target subunit 1 (MYPT), which results in the inhibition of the Hippo signaling pathway. This inhibition ultimately triggers gene transcription and cell proliferation through the YAP/TAZ transcriptional co-activators. 2) HSP 90 functions as a chaperone aiding in the stabilization of fibronectin. This support leads to the conversion of soluble fibronectin into an insoluble form. The insoluble fibronectin, in turn, plays a role in initiating cell invasion and metastasis by activating a series of pathways, including FAK, ILK, ERK, PI3K, and NF-κB cascades

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