Bornlisy Attenuates Colitis-Associated Colorectal Cancer via Inhibiting GPR43-Mediated Glycolysis.
Bornlisy Attenuates Colitis-Associated Colorectal Cancer via Inhibiting GPR43-Mediated Glycolysis.
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Bornlisy 通过抑制 GPR43 介导的糖酵解来减轻结肠炎相关的结直肠癌
DOI：
10.3389/fnut.2021.706382
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发表时间：
2021
影响因子：
5
通讯作者：
Wang T
中科院分区：
文献类型：
--
作者：
Lu X;Qiao S;Peng C;Yan W;Xu Z;Qu J;Hou Y;Zhao S;Chen P;Wang T
有证据表明，益生菌对结直肠癌（CRC）具有广泛的抗肿瘤作用。但是，机制仍然晦涩。在这里，我们研究了三种益生菌对结肠炎相关结肠癌（CAC）和基本机制的bornlisy（BO） - 库托尾tail的影响。与同伴相比，用BO治疗CAC小鼠会导致肿瘤负荷减少。 BO还抑制了CRC细胞体外的增殖和转移。此外，BO通过下调糖酵解抑制细胞增殖。激活糖酵解逆转了BO在CAC小鼠中的保护作用。从机械上讲，BO给药促进了GPR43的激活，其次是其下游PLC-PKC-ERK途径，从而导致葡萄糖代谢降低。这些结果表明，BO可以为CRC治疗提供干预策略，而GPR43是BO治疗过程中潜在的靶向受体。
There is evidence that probiotics have a broad antitumor effect in colorectal cancer (CRC). However, the mechanism remains obscure. Here, we investigated the effect of Bornlisy (BO)-cocktails of three probiotics on colitis-associated colon cancer (CAC) and the underlying mechanism. The treatment of CAC mice with BO resulted in decreased tumor loads as compared with their counterparts. BO also inhibited the proliferation and metastasis of CRC cells in vitro. Furthermore, BO inhibited cell proliferation through downregulating glycolysis. Activating glycolysis reversed the protective role of BO in the CAC mice. Mechanically, BO administration promoted the activation of GPR43, followed by its downstream PLC-PKC-ERK pathway, which led to decreased glucose metabolism. These results suggest that BO may provide an intervention strategy for CRC therapy, while GPR43 is a potential targeting receptor during the BO treatment.
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影响因子：
29.4
作者：
Chen X;Fruehauf J;Goldsmith JD;Xu H;Katchar KK;Koon HW;Zhao D;Kokkotou EG;Pothoulakis C;Kelly CP
通讯作者：
Kelly CP
DOI：
10.3322/caac.21398
发表时间：
2017-07-08
期刊：
CA: a cancer journal for clinicians
影响因子：
--
作者：
Bhatt AP;Redinbo MR;Bultman SJ
通讯作者：
Bultman SJ
影响因子：
30.8
作者：
Huyghe, Jeroen R.;Bien, Stephanie A.;Peters, Ulrike
通讯作者：
Peters, Ulrike
影响因子：
4.8
作者：
Brown, AJ;Goldsworthy, SM;Dowell, SJ
通讯作者：
Dowell, SJ
影响因子：
29.4
作者：
Dekker, Evelien;Rex, Douglas K.
通讯作者：
Rex, Douglas K.