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circNDUFB2 inhibits non-small cell lung cancer progression via destabilizing IGF2BPs and activating anti-tumor

Botai Li1, Lili Zhu1, Chunlai Lu2

  • 1State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Biomedical Engineering, 200032, Shanghai, China.

Nature Communications
|January 13, 2021
PubMed

Insights

Circular RNA NDUFB2 (circNDUFB2) is downregulated in non-small cell lung cancer (NSCLC). Restoring circNDUFB2 inhibits tumor growth and metastasis by degrading IGF2BPs and activating anti-tumor immunity.

Area of Science:

  • Oncology
  • Molecular Biology
  • Immunology

Background:

  • Circular RNAs (circRNAs) are increasingly recognized for their roles in cancer.
  • Non-small cell lung cancer (NSCLC) is a major cause of cancer-related mortality.
  • The specific functions of circRNAs in NSCLC progression remain incompletely understood.

Purpose of the Study:

  • To investigate the role of circNDUFB2 in non-small cell lung cancer (NSCLC).
  • To elucidate the molecular mechanisms underlying circNDUFB2's function in NSCLC.
  • To explore the potential of circNDUFB2 as a therapeutic target in NSCLC.

Main Methods:

  • Quantitative real-time PCR to assess circNDUFB2 expression levels in NSCLC tissues and cell lines.
  • Cellular assays to evaluate the effects of circNDUFB2 on NSCLC cell growth and metastasis.
  • Western blotting and immunoprecipitation to analyze protein-protein interactions and ubiquitination.
  • RNA immunoprecipitation followed by sequencing to identify circNDUFB2 binding proteins.
  • Analysis of immune cell infiltration in the tumor microenvironment.

Main Results:

  • circNDUFB2 was found to be downregulated in NSCLC tissues and negatively correlated with malignant features.
  • Overexpression of circNDUFB2 suppressed NSCLC cell growth and metastasis in vitro and in vivo.
  • circNDUFB2 acted as a scaffold, promoting the interaction between TRIM25 and IGF2BPs, leading to IGF2BP ubiquitination and degradation.
  • N6-methyladenosine (m6A) modification enhanced the TRIM25/circNDUFB2/IGF2BPs complex formation and IGF2BP degradation.
  • circNDUFB2 activated the RIG-I-MAVS signaling pathway, enhancing anti-tumor immunity by recruiting immune cells to the tumor microenvironment.

Conclusions:

  • circNDUFB2 functions as a tumor suppressor in NSCLC by inhibiting cell growth and metastasis.
  • circNDUFB2 exerts its tumor-suppressive effects through the TRIM25/IGF2BP axis and by activating anti-tumor immunity.
  • circNDUFB2 represents a potential therapeutic target for NSCLC treatment, modulating both tumor progression and immune responses.

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