CRKL promotes hepatocarcinoma through enhancing glucose metabolism of cancer cells via activating PI3K/Akt.
CRKL promotes hepatocarcinoma through enhancing glucose metabolism of cancer cells via activating PI3K/Akt.
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CRKL通过激活PI3K/Akt增强癌细胞葡萄糖代谢促进肝癌发生
DOI：
10.1111/jcmm.16303
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发表时间：
2021-03
影响因子：
5.3
通讯作者：
Sun MZ
中科院分区：
文献类型：
--
作者：
Guo C;Gao C;Lv X;Zhao D;Greenaway FT;Hao L;Tian Y;Liu S;Sun MZ
Abnormal glucose metabolism may contribute to cancer progression. As a member of the CRK (v‐crk sarcoma virus CT10 oncogene homologue) adapter protein family, CRKL (CRK‐like) associated with the development and progression of various tumours. However, the exact role and underlying mechanism of CRKL on energy metabolism remain unknown. In this study, we investigated the effect of CRKL on glucose metabolism of hepatocarcinoma cells. CRKL and PI3K were found to be overexpressed in both hepatocarcinoma cells and tissues; meanwhile, CRKL up‐regulation was positively correlated with PI3K up‐regulation. Functional investigations revealed that CRKL overexpression promoted glucose uptake, lactate production and glycogen synthesis of hepatocarcinoma cells by up‐regulating glucose transporters 1 (GLUT1), hexokinase II (HKII) expression and down‐regulating glycogen synthase kinase 3β (GSK3β) expression. Mechanistically, CRKL promoted glucose metabolism of hepatocarcinoma cells via enhancing the CRKL‐PI3K/Akt‐GLUT1/HKII‐glucose uptake, CRKL‐PI3K/Akt‐HKII‐glucose‐lactate production and CRKL‐PI3K/Akt‐Gsk3β‐glycogen synthesis. We demonstrate CRKL facilitates HCC malignancy via enhancing glucose uptake, lactate production and glycogen synthesis through PI3K/Akt pathway. It provides interesting fundamental clues to CRKL‐related carcinogenesis through glucose metabolism and offers novel therapeutic strategies for hepatocarcinoma.
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影响因子：
5.1
作者：
Luo, Fangxiu;Li, You;Zuo, Junli
通讯作者：
Zuo, Junli
CRKL过表达抑制小鼠肝癌Hca-P细胞的体外增殖、侵袭和迁移
影响因子：
7.5
作者：
Lin, Qiuyue;Sun, Ming-Zhong;Liu, Shuqing
通讯作者：
Liu, Shuqing
影响因子：
8.8
作者：
Martin SA;Souder DC;Miller KN;Clark JP;Sagar AK;Eliceiri KW;Puglielli L;Beasley TM;Anderson RM
通讯作者：
Anderson RM
影响因子：
5.2
作者：
Bonatelli, Murilo;Silva, Eduardo C. A.;Pinheiro, Celine
通讯作者：
Pinheiro, Celine
影响因子：
14.5
作者：
Mathupala SP;Ko YH;Pedersen PL
通讯作者：
Pedersen PL