<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Garofano K</submitter><funding>NCI NIH HHS</funding><funding>National Institutes of Health</funding><funding>NIH HHS</funding><pagination>2864</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9938282</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>13(1)</volume><pubmed_abstract>Platelets play a crucial role in cancer and thrombosis. However, the receptor-ligand repertoire mediating prostate cancer (PCa) cell-platelet interactions and ensuing consequences have not been fully elucidated. Microvilli emanating from the plasma membrane of PCa cell lines (RC77 T/E, MDA PCa 2b) directly contacted individual platelets and platelet aggregates. PCa cell-platelet interactions were associated with calcium mobilization in platelets, and translocation of P-selectin and integrin α&lt;sub>IIb&lt;/sub>β&lt;sub>3&lt;/sub> onto the platelet surface. PCa cell-platelet interactions reciprocally promoted PCa cell invasion and apoptotic resistance, and these events were insensitive to androgen receptor blockade by bicalutamide. PCa cells were exceedingly sensitive to activation by platelets in vit</pubmed_abstract><journal>Scientific reports</journal><pubmed_title>Prostate cancer cell-platelet bidirectional signaling promotes calcium mobilization, invasion and apoptotic resistance via distinct receptor-ligand pairs.</pubmed_title><pmcid>PMC9938282</pmcid><funding_grant_id>T32CA247756</funding_grant_id><funding_grant_id>T32 CA247756</funding_grant_id><funding_grant_id>U54MD010723</funding_grant_id><funding_grant_id>R01 CA204806</funding_grant_id><funding_grant_id>R01NS126090</funding_grant_id><pubmed_authors>Garofano K</pubmed_authors><pubmed_authors>Lee NH</pubmed_authors><pubmed_authors>Sidahmed A</pubmed_authors><pubmed_authors>Gordon O</pubmed_authors><pubmed_authors>Suwunnakorn S</pubmed_authors><pubmed_authors>Maggirwar SB</pubmed_authors><pubmed_authors>Rashid K</pubmed_authors><pubmed_authors>Popratiloff A</pubmed_authors><pubmed_authors>Brantner C</pubmed_authors><pubmed_authors>Perera MA</pubmed_authors><pubmed_authors>Smith M</pubmed_authors><pubmed_authors>O'Brien TJ</pubmed_authors><pubmed_authors>Horvath A</pubmed_authors><pubmed_authors>Rhim J</pubmed_authors><pubmed_authors>Diemert D</pubmed_authors><pubmed_authors>Khan S</pubmed_authors></additional><is_claimable>false</is_claimable><name>Prostate cancer cell-platelet bidirectional signaling promotes calcium mobilization, invasion and apoptotic resistance via distinct receptor-ligand pairs.</name><description>Platelets play a crucial role in cancer and thrombosis. However, the receptor-ligand repertoire mediating prostate cancer (PCa) cell-platelet interactions and ensuing consequences have not been fully elucidated. Microvilli emanating from the plasma membrane of PCa cell lines (RC77 T/E, MDA PCa 2b) directly contacted individual platelets and platelet aggregates. PCa cell-platelet interactions were associated with calcium mobilization in platelets, and translocation of P-selectin and integrin α&lt;sub>IIb&lt;/sub>β&lt;sub>3&lt;/sub> onto the platelet surface. PCa cell-platelet interactions reciprocally promoted PCa cell invasion and apoptotic resistance, and these events were insensitive to androgen receptor blockade by bicalutamide. PCa cells were exceedingly sensitive to activation by platelets in vit</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Feb</publication><modification>2026-07-14T20:07:00.428Z</modification><creation>2025-04-19T02:45:05.74Z</creation></dates><accession>S-EPMC9938282</accession><cross_references><pubmed>36806315</pubmed><doi>10.1038/s41598-023-29450-x</doi></cross_references></HashMap>