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. 2022 Jan 12;14(2):363. doi: 10.3390/cancers14020363

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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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(A) DU145 cell number in response to integrin blockade. Tumor cells were grown in 2 or 10% FBS and in the presence or without IGF-1. Untreated cells served as controls. Cell number was evaluated after 24, 48, and 72 h by the MTT assay. (B) Chemotactic movement of DU145 cells after blockade through monoclonal antibodies (specific blockade against α3, αV, or β1) with or without IGF-1 activation. (C) Adhesion modulation of DU145 through integrin β1 blockade in the presence of 2 versus 10% FBS. (B,C) are related to the non-blocked controls set to 100%. Error bars indicate standard deviation. Experiments were repeated three times. One representative experiment is shown. * indicates p < 0.05.

(A) DU145 cell number in response to integrin blockade. Tumor cells were grown in 2 or 10% FBS and in the presence or without IGF-1. Untreated cells served as controls. Cell number was evaluated after 24, 48, and 72 h by the MTT assay. (B) Chemotactic movement of DU145 cells after blockade through monoclonal antibodies (specific blockade against α3, αV, or β1) with or without IGF-1 activation. (C) Adhesion modulation of DU145 through integrin β1 blockade in the presence of 2 versus 10% FBS. (B,C) are related to the non-blocked controls set to 100%. Error bars indicate standard deviation. Experiments were repeated three times. One representative experiment is shown. * indicates p < 0.05.