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CD36 inhibits β-catenin/c-myc-mediated glycolysis through ubiquitination of GPC4 to repress colorectal tumorigenesis

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Listed:
  • Yuan Fang

    (Southern Medical University)

  • Zhi-Yong Shen

    (Southern Medical University)

  • Yi-Zhi Zhan

    (Southern Medical University
    Southern Medical University)

  • Xiao-Chuang Feng

    (Southern Medical University)

  • Ke-Li Chen

    (Southern Medical University)

  • Yong-Sheng Li

    (Southern Medical University)

  • Hai-Jun Deng

    (Southern Medical University)

  • Su-Ming Pan

    (Yue Bei People’s Hospital)

  • De-Hua Wu

    (Southern Medical University)

  • Yi Ding

    (Southern Medical University)

Abstract

The diverse expression pattern of CD36 reflects its multiple cellular functions. However, the roles of CD36 in colorectal cancer (CRC) remain unknown. Here, we discover that CD36 expression is progressively decreased from adenomas to carcinomas. CD36 loss predicts poor survival of CRC patients. In CRC cells, CD36 acts as a tumor suppressor and inhibits aerobic glycolysis in vitro and in vivo. Mechanically, CD36-Glypcian 4 (GPC4) interaction could promote the proteasome-dependent ubiquitination of GPC4, followed by inhibition of β-catenin/c-myc signaling and suppression of downstream glycolytic target genes GLUT1, HK2, PKM2 and LDHA. Moreover, disruption of CD36 in inflammation-induced CRC model as well as ApcMin/+ mice model significantly increased colorectal tumorigenesis. Our results reveal a CD36-GPC4-β-catenin-c-myc signaling axis that regulates glycolysis in CRC development and may provide an intervention strategy for CRC prevention.

Suggested Citation

  • Yuan Fang & Zhi-Yong Shen & Yi-Zhi Zhan & Xiao-Chuang Feng & Ke-Li Chen & Yong-Sheng Li & Hai-Jun Deng & Su-Ming Pan & De-Hua Wu & Yi Ding, 2019. "CD36 inhibits β-catenin/c-myc-mediated glycolysis through ubiquitination of GPC4 to repress colorectal tumorigenesis," Nature Communications, Nature, vol. 10(1), pages 1-16, December.
    • Handle: RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-11662-3
    DOI: 10.1038/s41467-019-11662-3
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    Cited by:

    1. Sheng Qiu & Qinan Wu & Hao Wang & Dongfang Liu & Chen Chen & Zhiming Zhu & Hongting Zheng & Gangyi Yang & Ling Li & Mengliu Yang, 2024. "AZGP1 in POMC neurons modulates energy homeostasis and metabolism through leptin-mediated STAT3 phosphorylation," Nature Communications, Nature, vol. 15(1), pages 1-18, December.
    2. Ping Yang & Hong Qin & Yiyu Li & Anhua Xiao & Enze Zheng & Han Zeng & Chunxiao Su & Xiaoqing Luo & Qiannan Lu & Meng Liao & Lei Zhao & Li Wei & Zac Varghese & John F. Moorhead & Yaxi Chen & Xiong Z. R, 2022. "CD36-mediated metabolic crosstalk between tumor cells and macrophages affects liver metastasis," Nature Communications, Nature, vol. 13(1), pages 1-16, December.

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