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. 2022 May 24;23(11):5874. doi: 10.3390/ijms23115874

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© 2022 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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Proposed model for the effect of SPARC on E-cadherin expression and migration mediated by integrin α_vβ₃ and the transcription factor ZEB1 in prostate cancer cells. (A) SPARC induces functional changes associated with the epithelial–mesenchymal transition (EMT): increased mesenchymal phenotype and enhanced motility. (B) Because SPARC requires the activity of integrin α_vβ₃ to induce E-cadherin downregulation and cell migration, SPARC effect could be a result of the direct or indirect association of SPARC and the integrin α_vβ₃. Through integrin α_vβ₃, SPARC could activate the focal adhesion kinase (FAK) and the integrin-linked kinase (ILK). FAK activation by phosphorylation on Y925 promotes focal adhesion turnover, enhancing motility. On the other hand, through FAK, ILK, or other downstream molecules, SPARC could be promoting the expression of the EMT transcription factor ZEB1. The transcription factor ZEB1 inhibits the expression of E-cadherin and induces the expression of mesenchymal markers such as vimentin.