嘌呤核苷酸可用性通过 Rheb GTPase 调节 mTORC1 活性。

Purine Nucleotide Availability Regulates mTORC1 Activity through the Rheb GTPase.

机构信息

Oncology R&D Group, Pfizer Worldwide Research and Development, 401 N. Middletown Road, Pearl River, NY 10965, USA.

Oncology R&D Group, Pfizer Worldwide Research and Development, 10646 Science Center Drive/CB4, San Diego, CA 92121, USA.

出版信息

Cell Rep. 2017 Jun 27;19(13):2665-2680. doi: 10.1016/j.celrep.2017.05.043.

Abstract

Pharmacologic agents that interfere with nucleotide metabolism constitute an important class of anticancer agents. Recent studies have demonstrated that mTOR complex 1 (mTORC1) inhibitors suppress de novo biosynthesis of pyrimidine and purine nucleotides. Here, we demonstrate that mTORC1 itself is suppressed by drugs that reduce intracellular purine nucleotide pools. Cellular treatment with AG2037, an inhibitor of the purine biosynthetic enzyme GARFT, profoundly inhibits mTORC1 activity via a reduction in the level of GTP-bound Rheb, an obligate upstream activator of mTORC1, because of a reduction in intracellular guanine nucleotides. AG2037 treatment provokes both mTORC1 inhibition and robust tumor growth suppression in mice bearing non-small-cell lung cancer (NSCLC) xenografts. These results indicate that alterations in purine nucleotide availability affect mTORC1 activity and suggest that inhibition of mTORC1 contributes to the therapeutic effects of purine biosynthesis inhibitors.

摘要

干扰核苷酸代谢的药物是一类重要的抗癌药物。最近的研究表明,mTOR 复合物 1(mTORC1)抑制剂可抑制嘧啶和嘌呤核苷酸的从头合成。在这里,我们证明 mTORC1 本身受到降低细胞内嘌呤核苷酸池的药物的抑制。细胞用嘌呤生物合成酶 GARFT 的抑制剂 AG2037 处理,通过降低 mTORC1 的必需上游激活剂 Rheb 的 GTP 结合水平,极大地抑制 mTORC1 活性,因为细胞内鸟嘌呤核苷酸减少。AG2037 处理在携带非小细胞肺癌(NSCLC)异种移植物的小鼠中既引起 mTORC1 抑制又引起强烈的肿瘤生长抑制。这些结果表明嘌呤核苷酸可用性的改变会影响 mTORC1 的活性,并表明 mTORC1 的抑制有助于嘌呤生物合成抑制剂的治疗效果。

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