2. Academic Validation
  3. LncRNA SNHG26 promotes gastric cancer progression and metastasis by inducing c-Myc protein translation and an energy metabolism positive feedback loop

LncRNA SNHG26 promotes gastric cancer progression and metastasis by inducing c-Myc protein translation and an energy metabolism positive feedback loop

  • Cell Death Dis. 2024 Mar 29;15(3):236. doi: 10.1038/s41419-024-06607-8.
Zhen-Hua Wu # 1 2,  Yi-Xuan Wang # 1 2,  Jun-Jiao Song # 2 3,  Li-Qin Zhao 4,  Yu-Jia Zhai 1 2,  Yan-Fang Liu 2 3,  Wei-Jian Guo 5 6
Affiliations

Affiliations

  • 1 Department of Medical Oncology, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
  • 2 Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
  • 3 Fudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Shanghai, 200032, China.
  • 4 Department of Oncology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
  • 5 Department of Medical Oncology, Fudan University Shanghai Cancer Center, Shanghai, 200032, China. guoweijian1@hotmail.com.
  • 6 Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China. guoweijian1@hotmail.com.
  • # Contributed equally.
PMID: 38553452 DOI: 10.1038/s41419-024-06607-8
Abstract

Metastasis is a bottleneck in Cancer treatment. Studies have shown the pivotal roles of long noncoding RNAs (lncRNAs) in regulating Cancer metastasis; however, our understanding of lncRNAs in gastric Cancer (GC) remains limited. RNA-seq was performed on metastasis-inclined GC tissues to uncover metastasis-associated lncRNAs, revealing upregulated small nucleolar RNA host gene 26 (SNHG26) expression, which predicted poor GC patient prognosis. Functional experiments revealed that SNHG26 promoted cellular epithelial-mesenchymal transition and proliferation in vitro and in vivo. Mechanistically, SNHG26 was found to interact with nucleolin (NCL), thereby modulating c-Myc expression by increasing its translation, and in turn promoting energy metabolism via Hexokinase 2 (HK2), which facilitates GC malignancy. The increase in energy metabolism supplies sufficient energy to promote c-Myc translation and expression, forming a positive feedback loop. In addition, metabolic and translation inhibitors can block this loop, thus inhibiting cell proliferation and mobility, indicating potential therapeutic prospects in GC.

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