Inhibition of Tumor Progression through the Coupling of Bacterial Respiration with Tumor Metabolism
Inhibition of Tumor Progression through the Coupling of Bacterial Respiration with Tumor Metabolism
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DOI：
10.1002/anie.202002649
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发表时间：
2020-09-15
影响因子：
16.6
通讯作者：
Zhang, Xian-Zheng
中科院分区：
文献类型：
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作者：
Chen, Qi-Wen;Wang, Jia-Wei;Zhang, Xian-Zheng
利用希瓦氏菌MR-1（S. oneidensisMR-1）通过将电子传递给金属矿物质进行呼吸来厌氧分解代谢乳酸，通过在S.一个密度为MR-1表面。Bac@MnO（2）生物杂化材料利用修饰的MnO（2）纳米花作为电子受体，肿瘤代谢产物乳酸作为电子供体，在肿瘤部位形成完整的细菌呼吸途径，导致细胞间乳酸的持续催化。此外，修饰的MnO（2）纳米花还可以催化内源性过氧化氢（H2 O2）转化为产生的氧气（O-2），这可以通过下调缺氧诱导因子-1 α（HIF-1 α）的表达来防止乳酸盐的产生。由于乳酸在肿瘤发展中起着关键作用，生物杂化材料Bac@MnO（2）可以通过将细菌呼吸与肿瘤代谢偶联来显著抑制肿瘤进展。
By leveraging the ability ofShewanella oneidensisMR-1 (S. oneidensisMR-1) to anaerobically catabolize lactate through the transfer of electrons to metal minerals for respiration, a lactate-fueled biohybrid (Bac@MnO2) was constructed by modifying manganese dioxide (MnO2) nanoflowers on theS. oneidensisMR-1 surface. The biohybrid Bac@MnO(2)uses decorated MnO(2)nanoflowers as electron receptor and the tumor metabolite lactate as electron donor to make a complete bacterial respiration pathway at the tumor sites, which results in the continuous catabolism of intercellular lactate. Additionally, decorated MnO(2)nanoflowers can also catalyze the conversion of endogenous hydrogen peroxide (H2O2) into generate oxygen (O-2), which could prevent lactate production by downregulating hypoxia-inducible factor-1 alpha (HIF-1 alpha) expression. As lactate plays a critical role in tumor development, the biohybrid Bac@MnO(2)could significantly inhibit tumor progression by coupling bacteria respiration with tumor metabolism.