<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>6(1)</volume><submitter>da Silva IA</submitter><pubmed_abstract>A major drawback of radiotherapy is the accelerated growth of the surviving tumor cells. Radiotherapy generates a variety of lipids that bind to the receptor for platelet-activating factor, expressed by cells in the tumor microenvironment. In the present study, using the TC-1 tumor cell line, we found that irradiation induced a twofold increase in receptor expression and generated agonists of receptor. Irradiated cells induced a 20-fold increase in live TC-1 proliferation in vitro. Furthermore, subcutaneous co-injection of irradiated TC-1 cells with TC-1 expressing luciferase (TC-1 fluc&lt;sup>+&lt;/sup>) markedly increased TC-1 fluc&lt;sup>+&lt;/sup> proliferation in a receptor-dependent way. Moreover we used a human carcinoma cell line not expressing the PAF receptor (KBM) and the same cell transfected with the receptor gene (KBP). Following co-injection of live KBP cells with irradiated KBM in RAG mice, the tumor growth was significantly increased compared with tumor formed following co-injection of live KBM with irradiated KBM. This tumor cell repopulation correlated with increased infiltration of tumor-promoting macrophages (CD206+). We propose that receptor represents a possible target for improving the efficacy of radiotherapy through inhibition of tumor repopulation.</pubmed_abstract><journal>Oncogenesis</journal><pagination>e296</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5294253</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Platelet-activating factor (PAF) receptor as a promising target for cancer cell repopulation after radiotherapy.</pubmed_title><pmcid>PMC5294253</pmcid><pubmed_authors>Lepique AP</pubmed_authors><pubmed_authors>da Silva IA</pubmed_authors><pubmed_authors>Jancar S</pubmed_authors><pubmed_authors>Chammas R</pubmed_authors></additional><is_claimable>false</is_claimable><name>Platelet-activating factor (PAF) receptor as a promising target for cancer cell repopulation after radiotherapy.</name><description>A major drawback of radiotherapy is the accelerated growth of the surviving tumor cells. Radiotherapy generates a variety of lipids that bind to the receptor for platelet-activating factor, expressed by cells in the tumor microenvironment. In the present study, using the TC-1 tumor cell line, we found that irradiation induced a twofold increase in receptor expression and generated agonists of receptor. Irradiated cells induced a 20-fold increase in live TC-1 proliferation in vitro. Furthermore, subcutaneous co-injection of irradiated TC-1 cells with TC-1 expressing luciferase (TC-1 fluc&lt;sup>+&lt;/sup>) markedly increased TC-1 fluc&lt;sup>+&lt;/sup> proliferation in a receptor-dependent way. Moreover we used a human carcinoma cell line not expressing the PAF receptor (KBM) and the same cell transfected with the receptor gene (KBP). Following co-injection of live KBP cells with irradiated KBM in RAG mice, the tumor growth was significantly increased compared with tumor formed following co-injection of live KBM with irradiated KBM. This tumor cell repopulation correlated with increased infiltration of tumor-promoting macrophages (CD206+). We propose that receptor represents a possible target for improving the efficacy of radiotherapy through inhibition of tumor repopulation.</description><dates><release>2017-01-01T00:00:00Z</release><publication>2017 Jan</publication><modification>2025-04-22T19:19:03.736Z</modification><creation>2019-03-27T02:35:52Z</creation></dates><accession>S-EPMC5294253</accession><cross_references><pubmed>28134937</pubmed><doi>10.1038/oncsis.2016.90</doi></cross_references></HashMap>