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LncRNA GLCC1 promotes colorectal carcinogenesis and glucose metabolism by stabilizing c-Myc

Author

Listed:
  • Jiayin Tang

    (Shanghai Jiao Tong University
    Shanghai Jiao Tong University)

  • Tingting Yan

    (Shanghai Jiao Tong University)

  • Yujie Bao

    (Shanghai Jiao Tong University
    Shanghai Jiao Tong University School of Medicine)

  • Chaoqin Shen

    (Shanghai Jiao Tong University)

  • Chenyang Yu

    (Shanghai Jiao Tong University)

  • Xiaoqiang Zhu

    (Shanghai Jiao Tong University)

  • Xianglong Tian

    (Shanghai Jiao Tong University)

  • Fangfang Guo

    (Shanghai Jiao Tong University)

  • Qian Liang

    (Shanghai Jiao Tong University)

  • Qiang Liu

    (Shanghai Jiao Tong University School of Medicine)

  • Ming Zhong

    (Shanghai Jiao Tong University)

  • Jinxian Chen

    (Shanghai Jiao Tong University)

  • Zhizheng Ge

    (Shanghai Jiao Tong University)

  • Xiaobo Li

    (Shanghai Jiao Tong University)

  • Xiaoyu Chen

    (Shanghai Jiao Tong University)

  • Yun Cui

    (Shanghai Jiao Tong University)

  • Yingxuan Chen

    (Shanghai Jiao Tong University)

  • Weiping Zou

    (University of Michigan School of Medicine)

  • Haoyan Chen

    (Shanghai Jiao Tong University)

  • Jie Hong

    (Shanghai Jiao Tong University)

  • Jing-Yuan Fang

    (Shanghai Jiao Tong University)

Abstract

Long non-coding RNAs (lncRNAs) contribute to colorectal cancer (CRC). However, the role of lncRNAs in CRC metabolism, especially glucose metabolism remains largely unknown. In this study, we identify a lncRNA, GLCC1, which is significantly upregulated under glucose starvation in CRC cells, supporting cell survival and proliferation by enhancing glycolysis. Mechanistically, GLCC1 stabilizes c-Myc transcriptional factor from ubiquitination by direct interaction with HSP90 chaperon and further specifies the transcriptional modification pattern on c-Myc target genes, such as LDHA, consequently reprogram glycolytic metabolism for CRC proliferation. Clinically, GLCC1 is associated with tumorigenesis, tumor size and predicts poor prognosis. Thus, GLCC1 is mechanistically, functionally, and clinically oncogenic in colorectal cancer. Targeting GLCC1 and its pathway may be meaningful for treating patients with colorectal cancer.

Suggested Citation

  • Jiayin Tang & Tingting Yan & Yujie Bao & Chaoqin Shen & Chenyang Yu & Xiaoqiang Zhu & Xianglong Tian & Fangfang Guo & Qian Liang & Qiang Liu & Ming Zhong & Jinxian Chen & Zhizheng Ge & Xiaobo Li & Xia, 2019. "LncRNA GLCC1 promotes colorectal carcinogenesis and glucose metabolism by stabilizing c-Myc," Nature Communications, Nature, vol. 10(1), pages 1-15, December.
    • Handle: RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-11447-8
    DOI: 10.1038/s41467-019-11447-8
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    Cited by:

    1. Xueman Chen & Rong Luo & Yunmei Zhang & Shuying Ye & Xin Zeng & Jiang Liu & Di Huang & Yujie Liu & Qiang Liu & Man-Li Luo & Erwei Song, 2022. "Long noncoding RNA DIO3OS induces glycolytic-dominant metabolic reprogramming to promote aromatase inhibitor resistance in breast cancer," Nature Communications, Nature, vol. 13(1), pages 1-19, December.

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