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Improvement of purine and pyrimidine antimetabolite-based anticancer treatment by selective suppression of mycoplasma-encoded catabolic enzymes

机译:通过选择性抑制支原体编码的分解代谢酶改善嘌呤和嘧啶类抗代谢物的抗癌治疗

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摘要

Most mycoplasmas are present as commensals, colonising the mucosa of our respiratory and gastrointestinal tract. Experimental data suggest that the long-term association of certain mycoplasma species with mammalian cells might favour host-cell transformation and malignancy. Moreover, increased mycoplasma infection has been noted in several cancers. Despite efforts to develop target-specific anticancer drugs, current cancer treatment still relies on the use of nucleobase or nucleoside-based analogues. Here, we provide experimental evidence that nucleoside-metabolising catabolic enzymes expressed by mycoplasmas substantially compromise the efficacy of nucleoside antimetabolites used in the treatment of cancer. We also suggest potential methods for improving future chemotherapy by suppressing mycoplasma-mediated catabolism of the anticancer nucleoside analogues.
机译:大多数支原体以共生形式存在,定植在我们的呼吸道和胃肠道的粘膜上。实验数据表明某些支原体物种与哺乳动物细胞的长期联系可能有利于宿主细胞转化和恶性肿瘤。此外,已经注意到在几种癌症中支原体感染增加。尽管开发了针对靶标的抗癌药物,但当前的癌症治疗仍然依赖于使用核碱基或基于核苷的类似物。在这里,我们提供实验证据,支原体表达的核苷代谢分解代谢酶大大损害了用于治疗癌症的核苷抗代谢物的功效。我们还建议了通过抑制支原体介导的抗癌核苷类似物的分解代谢来改善未来化学疗法的潜在方法。

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