Transketolase promotes colorectal cancer metastasis through regulating AKT phosphorylation.
Transketolase promotes colorectal cancer metastasis through regulating AKT phosphorylation.
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DOI：
10.1038/s41419-022-04575-5
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发表时间：
2022-02-02
影响因子：
9
通讯作者：
Bai J
中科院分区：
文献类型：
--
作者：
Li M;Zhao X;Yong H;Xu J;Qu P;Qiao S;Hou P;Li Z;Chu S;Zheng J;Bai J
转酮醇酶(TKT)是磷酸戊糖途径(PPP)中的重要代谢酶，参与维持5-磷酸核糖水平。TKT是维持细胞生长所必需的。然而，我们发现，除此之外，TKT还可以通过其他途径影响肿瘤的进展。我们先前的研究表明，TKT可能通过影响胆汁酸代谢来促进肝癌的发展。在本研究中，我们发现TKT在结直肠癌中的表达显著上调，TKT的异常高表达与结直肠癌的预后不良有关。此外，TKT还促进了结直肠癌细胞的生长和转移。进一步研究表明，TKT与GRP78相互作用，通过增加AKT的磷酸化促进结直肠癌细胞的糖酵解，从而促进结直肠癌细胞的转移。因此，TKT有望成为判断结直肠癌预后的指标，并为结直肠癌新治疗靶点的药物开发提供理论依据。
Transketolase (TKT) which is an important metabolic enzyme in the pentose phosphate pathway (PPP) participates in maintaining ribose 5-phosphate levels. TKT is necessary for maintaining cell growth. However, we found that in addition to this, TKT can also affect tumor progression through other ways. Our previous study indicate that TKT could promote the development of liver cancer by affecting bile acid metabolism. And in this study, we discovered that TKT expression was remarkably upregulated in colorectal cancer, abnormal high expression of TKT is associated with poor prognosis of colorectal cancer. Additionally, TKT promoted colorectal cancer cell growth and metastasis. Further study demonstrated that TKT interacted with GRP78 and promoted colorectal cancer cell glycolysis through increasing AKT phosphorylation, thereby enhancing colorectal cancer cell metastasis. Thus, TKT is expected to become an indicator for judging the prognosis of colorectal cancer, and provide a theoretical basis for drug development of new treatment targets for colorectal cancer.
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DOI：
10.1016/s0360-3016(01)01630-3
发表时间：
2001-10-01
影响因子：
7
作者：
Brizel, DM;Schroeder, T;Mueller-Klieser, W
通讯作者：
Mueller-Klieser, W
影响因子：
4.4
作者：
Coy, JF;Dubel, S;Poustka, A
通讯作者：
Poustka, A
影响因子：
3.1
作者：
Mhaidat, Nizar M.;Alzoubi, Karem H.;Khabour, Omar F.
通讯作者：
Khabour, Omar F.
影响因子：
4
作者：
Ricciardelli, Carmela;Lokman, Noor A.;Oehler, Martin K.
通讯作者：
Oehler, Martin K.
影响因子：
7.5
作者：
Mao, Li-jun;Yang, Chun-hua;Shan, Yu-xi
通讯作者：
Shan, Yu-xi