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Loss of the fructose transporter SLC2A5 inhibits cancer cell migration.
Groenendyk, Jody; Stoletov, Konstantin; Paskevicius, Tautvydas; Li, Wenjuan; Dai, Ning; Pujol, Myriam; Busaan, Erin; Ng, Hoi Hei; Boukouris, Aristeidis E; Saleme, Bruno; Haromy, Alois; Cui, Kaisa; Hu, Miao; Yan, Yanan; Zhang, Rui; Michelakis, Evangelos; Chen, Xing-Zhen; Lewis, John D; Tang, Jingfeng; Agellon, Luis B; Michalak, Marek.
Affiliation
  • Groenendyk J; Department of Biochemistry, University of Alberta, Edmonton, AB, Canada.
  • Stoletov K; Department of Oncology, University of Alberta, Edmonton, AB, Canada.
  • Paskevicius T; Department of Biochemistry, University of Alberta, Edmonton, AB, Canada.
  • Li W; Department of Biochemistry, University of Alberta, Edmonton, AB, Canada.
  • Dai N; Department of Biochemistry, University of Alberta, Edmonton, AB, Canada.
  • Pujol M; Department of Biochemistry, University of Alberta, Edmonton, AB, Canada.
  • Busaan E; Department of Biochemistry, University of Alberta, Edmonton, AB, Canada.
  • Ng HH; Department of Biochemistry, University of Alberta, Edmonton, AB, Canada.
  • Boukouris AE; Department of Medicine, University of Alberta, Edmonton, AB, Canada.
  • Saleme B; Department of Medicine, University of Alberta, Edmonton, AB, Canada.
  • Haromy A; Department of Medicine, University of Alberta, Edmonton, AB, Canada.
  • Cui K; Wuxi Cancer Institute, Affiliated Hospital of Jiangnan University, Wuxi, Jiangsu, China.
  • Hu M; National "111" Center for Cellular Regulation and Molecular Pharmaceutics, Hubei University of Technology, Wuhan, China.
  • Yan Y; National "111" Center for Cellular Regulation and Molecular Pharmaceutics, Hubei University of Technology, Wuhan, China.
  • Zhang R; National "111" Center for Cellular Regulation and Molecular Pharmaceutics, Hubei University of Technology, Wuhan, China.
  • Michelakis E; Department of Medicine, University of Alberta, Edmonton, AB, Canada.
  • Chen XZ; Department of Physiology, University of Alberta, Edmonton, AB, Canada.
  • Lewis JD; Department of Oncology, University of Alberta, Edmonton, AB, Canada.
  • Tang J; National "111" Center for Cellular Regulation and Molecular Pharmaceutics, Hubei University of Technology, Wuhan, China.
  • Agellon LB; School of Human Nutrition, McGill University, Montreal, QC, Canada.
  • Michalak M; Department of Biochemistry, University of Alberta, Edmonton, AB, Canada.
Front Cell Dev Biol ; 10: 896297, 2022.
Article in En | MEDLINE | ID: mdl-36268513
Metastasis is the primary cause of cancer patient death and the elevation of SLC2A5 gene expression is often observed in metastatic cancer cells. Here we evaluated the importance of SLC2A5 in cancer cell motility by silencing its gene. We discovered that CRISPR/Cas9-mediated inactivation of the SLC2A5 gene inhibited cancer cell proliferation and migration in vitro as well as metastases in vivo in several animal models. Moreover, SLC2A5-attenuated cancer cells exhibited dramatic alterations in mitochondrial architecture and localization, uncovering the importance of SLC2A5 in directing mitochondrial function for cancer cell motility and migration. The direct association of increased abundance of SLC2A5 in cancer cells with metastatic risk in several types of cancers identifies SLC2A5 as an important therapeutic target to reduce or prevent cancer metastasis.
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Full text: 1 Collection: 01-internacional Database: MEDLINE Language: En Journal: Front Cell Dev Biol Year: 2022 Type: Article Affiliation country: Canada
Fulltext
Print
XML
PubMed Links
Search on Google

Full text: 1 Collection: 01-internacional Database: MEDLINE Language: En Journal: Front Cell Dev Biol Year: 2022 Type: Article Affiliation country: Canada