CAV1/caveolin 1 enhances aerobic glycolysis in colon cancer cells via activation of SLC2A3/GLUT3 transcription

Tae Kyu Ha, Sung Gil Chi

Research output: Contribution to journalShort surveypeer-review

47 Citations (Scopus)


Although elevated expression of CAV1/caveolin 1 is associated with the malignant progression of various human cancers, the molecular mechanism underlying its oncogenic functions is largely unknown. We found that CAV1 is frequently overexpressed in advanced colorectal tumors due to aberrant promoter CpG site hypomethylation, and its elevation is implicated in enhanced aerobic glycolysis of tumor cells. Depletion of elevated CAV1 downregulates glucose uptake, intracellular ATP level and lactate accumulation, and triggers autophagy through activation of AMPK-TP53/p53 signaling. CAV1 elevation increases glucose uptake and ATP production by stimulating transcription of the glucose transporter SLC2A3/ GLUT3 via an HMGA1-binding site within the promoter. Collectively, our study suggests that elevated CAV1 expression may contribute to colorectal tumor progression by providing tumor cells growth and survival advantages under nutritional stress conditions.

Original languageEnglish
Pages (from-to)1684-1685
Number of pages2
Issue number11
Publication statusPublished - 2012 Nov

Bibliographical note

Funding Information:
This work was supported in part by grants from National Research Foundation of Korea (2009-0078864 and 2009-0087099) and the National Cancer Center (0820070), Republic of Korea.


  • Autophagy
  • Caveolin-1
  • Colon cancer
  • GLUT3
  • Glycolysis
  • HMGA1

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology


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