AI Article Synopsis
- Existing anticancer approaches targeting integrins in tumor cells have seen limited effectiveness, prompting the exploration of methods to enhance integrin pathways that inhibit tumor growth.
- A study created a model of metastatic prostate cancer where reducing the α3β1 integrin highlighted its role in signaling through Abl kinases, which limits harmful cell behaviors like migration and invasion.
- The findings suggest that α3 integrin-deficient prostate cancers might benefit from new therapies focusing on the Hippo pathway, revealing complex tumor-suppressing roles for Abl kinases in prostate cancer that could clarify why certain treatments have not worked in clinical trials.
Article Abstract
Existing anticancer strategies focused on disrupting integrin functions in tumor cells or tumor-involved endothelial cells have met limited success. An alternative strategy is to augment integrin-mediated pathways that suppress tumor progression, but how integrins can signal to restrain malignant behavior remains unclear. To address this issue, we generated an in vivo model of prostate cancer metastasis via depletion of α3β1 integrin, a correlation observed in a significant proportion of prostate cancers. Our data describe a mechanism whereby α3β1 signals through Abl family kinases to restrain Rho GTPase activity, support Hippo pathway suppressor functions, and restrain prostate cancer migration, invasion, and anchorage-independent growth. This α3β1-Abl kinase-Hippo suppressor pathway identified α3 integrin-deficient prostate cancers as potential candidates for Hippo-targeted therapies currently under development, suggesting new strategies for targeting metastatic prostate cancer based on integrin expression. Our data also revealed paradoxical tumor suppressor functions for Abl kinases in prostate cancer that may help to explain the failure of Abl kinase inhibitor imatinib in prostate cancer clinical trials. Cancer Res; 76(22); 6577-87. ©2016 AACR.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5290210 | PMC |
| http://dx.doi.org/10.1158/0008-5472.CAN-16-1483 | DOI Listing |
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