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首页> 外文期刊>Cytokine >Cervical cancer cells produce TGF-β1 through the CD73-adenosine pathway and maintain CD73 expression through the autocrine activity of TGF-β1
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Cervical cancer cells produce TGF-β1 through the CD73-adenosine pathway and maintain CD73 expression through the autocrine activity of TGF-β1

机译：宫颈癌细胞通过CD73-腺苷途径产生TGF-β1，并通过TGF-β1的自分泌活性维持CD73表达

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摘要

In cancer, the adenosinergic pathway participates in the generation of an immunosuppressive microenvironment and in the promotion of tumor growth through the generation of adenosine (Ado). The present study analyzed the participation of Ado, generated through the functional activity of the cervical cancer (CeCa) pathway in CeCa cells, to induce the expression and secretion of TGF-β1, as well as the participation of this factor to maintain CD73 expression. Ado concentrations greater than 10 uM were necessary to induce an increase of over 50% in the production and expression of TGF-β1 in CeCa tumor cells. Blockade of A2AR and A2BR with the specific antagonists, ZM241385 and MRS1754, respectively, strongly reversed the production of TGF-β1. TGF-β1 produced by CeCa cells was necessary to maintain CD73 expression because the addition of anti-TGF-p neutralizing antibodies or the inhibition of TGF-βRI strongly reversed the expression of CD73 in the CeCa cells. These results suggested a feedback loop in CeCa cells that favors immunosuppressive activity through the production of TGF-β1 and Ado as well as the autocrine activity of TGF-β1 and expression of CD73.
机译：在癌症中，腺苷能途径参与产生免疫抑制微环境和通过腺苷（ADO）的产生促进肿瘤生长。本研究分析了通过CECA细胞中宫颈癌（CECA）途径的功能活性产生的ADO的参与，诱导TGF-β1的表达和分泌，以及该因子的参与维持CD73表达。大于10μm的ADO浓度是在CECA肿瘤细胞中产生和表达诱导超过50％的增加。封锁A2AR和A2BR分别用特定的拮抗剂，ZM241385和MRS1754，强烈地逆转了TGF-β1的产生。 CECA细胞产生的TGF-β1是维持CD73表达所需的，因为添加抗TGF-P中和抗体或TGF-βRI的抑制强烈地反转CECA细胞中CD73的表达。这些结果表明CECA细胞中的反馈环，其通过生产TGF-β1和ADO以及TGF-β1的自分泌活性以及CD73的表达来解决免疫抑制活性。

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