Dergi makalesi Açık Erişim
Akgol, Sezer; Kalkan, Batuhan Mert; Yucel, Dogacan; Kocabas, Fatih
<?xml version='1.0' encoding='UTF-8'?> <record xmlns="http://www.loc.gov/MARC21/slim"> <leader>00000nam##2200000uu#4500</leader> <datafield tag="700" ind1=" " ind2=" "> <subfield code="a">Kalkan, Batuhan Mert</subfield> <subfield code="u">Koc Univ, Istanbul, Turkey</subfield> </datafield> <datafield tag="700" ind1=" " ind2=" "> <subfield code="a">Yucel, Dogacan</subfield> <subfield code="u">Univ Minnesota, Dept Med, Minneapolis, MN 55455 USA</subfield> </datafield> <datafield tag="700" ind1=" " ind2=" "> <subfield code="a">Kocabas, Fatih</subfield> <subfield code="u">Yeditepe Univ, Dept Genet & Bioengn, Fac Engn, Istanbul, Turkey</subfield> </datafield> <datafield tag="909" ind1="C" ind2="4"> <subfield code="p">VASCULAR PHARMACOLOGY</subfield> <subfield code="v">141</subfield> </datafield> <datafield tag="980" ind1=" " ind2=" "> <subfield code="a">user-tubitak-destekli-proje-yayinlari</subfield> </datafield> <datafield tag="540" ind1=" " ind2=" "> <subfield code="a">Creative Commons Attribution</subfield> <subfield code="u">http://www.opendefinition.org/licenses/cc-by</subfield> </datafield> <datafield tag="024" ind1=" " ind2=" "> <subfield code="a">10.1016/j.vph.2021.106903</subfield> <subfield code="2">doi</subfield> </datafield> <datafield tag="245" ind1=" " ind2=" "> <subfield code="a">SC1 limits tube formation, branching, migration, expansion and induce apoptosis of endothelial cells</subfield> </datafield> <datafield tag="100" ind1=" " ind2=" "> <subfield code="a">Akgol, Sezer</subfield> <subfield code="u">Yeditepe Univ, Dept Genet & Bioengn, Fac Engn, Istanbul, Turkey</subfield> </datafield> <datafield tag="909" ind1="C" ind2="O"> <subfield code="o">oai:aperta.ulakbim.gov.tr:238526</subfield> <subfield code="p">user-tubitak-destekli-proje-yayinlari</subfield> </datafield> <datafield tag="650" ind1="1" ind2="7"> <subfield code="2">opendefinition.org</subfield> <subfield code="a">cc-by</subfield> </datafield> <datafield tag="260" ind1=" " ind2=" "> <subfield code="c">2021-01-01</subfield> </datafield> <datafield tag="856" ind1="4" ind2=" "> <subfield code="u">https://aperta.ulakbim.gov.trrecord/238526/files/bib-c3e8c404-0599-49d3-b43e-aa41806730e7.txt</subfield> <subfield code="z">md5:5bf3950d96fe837c6eb8f36675b0fef6</subfield> <subfield code="s">190</subfield> </datafield> <datafield tag="542" ind1=" " ind2=" "> <subfield code="l">open</subfield> </datafield> <controlfield tag="005">20221007101451.0</controlfield> <controlfield tag="001">238526</controlfield> <datafield tag="980" ind1=" " ind2=" "> <subfield code="a">publication</subfield> <subfield code="b">article</subfield> </datafield> <datafield tag="520" ind1=" " ind2=" "> <subfield code="a">Endothelial cells (ECs) are essential in the growth and progression of the tumor cells by supplying nutrition and angiogenesis factors. Targeting ECs emerged as a major strategy to prevent the growth of tumors. Studies suggest that ERK1/2 signaling is important for endothelial cells, which could be specifically targeted by small molecule SC1. We aimed to study the effects of SC1 treatments on endothelial cell proliferation, angiogenesis, and death. To this end, we performed viability, apoptosis, cell cycle, gene expression, wound closure, tube formation, and western blot analysis in endothelial cells post SC1 treatments. Intriguingly, we found that SC1 has an antiangiogenic effect on endothelial cells, which limits the endothelial cell expansion, tube formation, branching, and migration. The proliferation is especially limited in dose dependent manner by SC1. In addition, we found that SC1 elevates the apoptosis of endothelial cells and associated pathways including BAK1, Stat1, Sox4, and Caspase1. We believe that these findings could contribute to the development of improved therapies based on the SC1 as an attractive candidate for anticancer clinical studies targeted to tumor angiogenesis.</subfield> </datafield> </record>
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