Potential role of NDRG2 in reprogramming cancer metabolism and epithelial-to-mesenchymal transition

被引:17
作者
Chen, Xiang-Liu [1 ]
Lei, Lan [1 ]
Hong, Lian-Lian [1 ]
Ling, Zhi-Qiang [1 ]
机构
[1] Zhejiang Canc Hosp, Zhejiang Canc Ctr, Zhejiang Canc Inst, 1 Banshan East Rd, Hangzhou 310022, Zhejiang, Peoples R China
基金
中国国家自然科学基金;
关键词
NDRG2 (N-MYC downstream-regulatedgene 2); Tumor suppressor gene; EMT (Epithelial-to-mesenchymal transition); Metastasis; Metabolic reprogramming; PYRUVATE-KINASE M2; GENE; 2; NDRG2; CELL-MIGRATION; POOR-PROGNOSIS; DOWNSTREAM; EXPRESSION; METASTASIS; GROWTH; TARGET; PHOSPHORYLATION;
D O I
10.14670/HH-11-957
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Epithelial-to-mesenchymal transition (EMT) allows a cell with epithelial characteristics to transdifferentiate into a cell with mesenchymal characteristics, which is recognized as a key priming event for the initiation and evolvement of cancer metastasis. Accumulating data has shown that aberrant cancer metabolism contributes to the execution of EMT and cancer metastasis through multiple pathological pathways. Recently, the N-MYC downstream-regulated gene 2 (NDRG2), as a tumor suppressor and metabolism-related gene in various cancers, has been widely noted. NDGR2 is associated with energy metabolism, especially glycose metabolism. Hence, we propose a hypothesis that EMT is repressed by NDRG2 via cancer metabolic reprogramming, and summarize the pathological processes and molecular pathways related to the regulation of NDRG2.
引用
收藏
页码:655 / 663
页数:9
相关论文
共 76 条
[1]  
[Anonymous], PLOS ONE
[2]   Attenuation of LDHA expression in cancer cells leads to redox-dependent alterations in cytoskeletal structure and cell migration [J].
Arseneault, Robert ;
Chien, Andrew ;
Newington, Jordan T. ;
Rappon, Tim ;
Harris, Richard ;
Cumming, Robert C. .
CANCER LETTERS, 2013, 338 (02) :255-266
[3]   miR-155 Drives Metabolic Reprogramming of ER+ Breast Cancer Cells Following Long-Term Estrogen Deprivation and Predicts Clinical Response to Aromatase Inhibitors [J].
Bacci, Marina ;
Giannoni, Elisa ;
Fearns, Antony ;
Ribas, Ricardo ;
Gao, Qiong ;
Taddei, Maria Letizia ;
Pintus, Gianfranco ;
Dowsett, Mitch ;
Isacke, Clare M. ;
Martin, Lesley-Ann ;
Chiarugi, Paola ;
Morandi, Andrea .
CANCER RESEARCH, 2016, 76 (06) :1615-1626
[4]   Cancer Cell Metabolism: One Hallmark, Many Faces [J].
Cantor, Jason R. ;
Sabatini, David M. .
CANCER DISCOVERY, 2012, 2 (10) :881-898
[5]   The effect of adenovirus-conjugated NDRG2 on p53-mediated apoptosis of hepatocarcinoma cells through attenuation of nucleotide excision repair capacity [J].
Cao, Wei ;
Zhang, Ju-liang ;
Feng, Da-yun ;
Liu, Xue-wu ;
Li, Yan ;
Wang, Li-feng ;
Ya, Li-bo ;
Zhang, Hongxin ;
Zhang, Jian .
BIOMATERIALS, 2014, 35 (03) :993-1003
[6]   Proteomic analysis of β-catenin activation in mouse liver by DIGE analysis identifies glucose metabolism as a new target of the Wnt pathway [J].
Chafey, Philippe ;
Finzi, Laetitia ;
Boisgard, Raphael ;
Cauezac, Michele ;
Clary, Guillem ;
Broussard, Cedric ;
Pegorier, Jean-Paul ;
Guillonneau, Francois ;
Mayeux, Patrick ;
Camoin, Luc ;
Tavitian, Bertrand ;
Colnot, Sabine ;
Perret, Christine .
PROTEOMICS, 2009, 9 (15) :3889-3900
[7]   Mammalian Target of Rapamycin (mTOR) Regulates Transforming Growth Factor-β1 (TGF-β1)-Induced Epithelial-Mesenchymal Transition via Decreased Pyruvate Kinase M2 (PKM2) Expression in Cervical Cancer Cells [J].
Cheng, Ke-yan ;
Hao, Min .
MEDICAL SCIENCE MONITOR, 2017, 23 :2017-2028
[8]   Metformin Inhibits TGF-β1-Induced Epithelial-to-Mesenchymal Transition via PKM2 Relative-mTOR/p70s6k Signaling Pathway in Cervical Carcinoma Cells [J].
Cheng, Keyan ;
Hao, Min .
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 2016, 17 (12)
[9]   Cellular Fatty Acid Metabolism and Cancer [J].
Currie, Erin ;
Schulze, Almut ;
Zechner, Rudolf ;
Walther, Tobias C. ;
Farese, Robert V., Jr. .
CELL METABOLISM, 2013, 18 (02) :153-161
[10]   MYC-Induced Cancer Cell Energy Metabolism and Therapeutic Opportunities [J].
Dang, Chi V. ;
Le, Anne ;
Gao, Ping .
CLINICAL CANCER RESEARCH, 2009, 15 (21) :6479-6483