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Oncogenic SLC2A11-MIF fusion protein interacts with polypyrimidine tract binding protein 1 to facilitate bladder

Liang Cheng1,2, Chenwei Yang1,2, Junlin Lu1,2

  • 1Department of Urology Sun Yat-sen Memorial Hospital, Sun Yat-sen University Guangzhou Guangdong China.

Medcomm
|August 19, 2024
PubMed

Insights

A novel bladder cancer fusion, solute carrier family 2-member 11 (SLC2A11) and macrophage migration inhibitory factor (MIF), promotes tumor growth and metastasis. This SLC2A11-MIF fusion protein interacts with PTBP1, regulating mRNA stability and cancer progression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genomics

Background:

  • Chimeric RNAs are emerging as therapeutic targets in cancer, but their functions are often unknown.
  • The specific roles and therapeutic potential of most fusion transcripts in cancer remain largely unexplored.
  • Identifying novel fusion transcripts is crucial for understanding cancer development and discovering new therapeutic strategies.

Purpose of the Study:

  • To identify and characterize a novel chimeric RNA, SLC2A11-MIF, in bladder cancer.
  • To investigate the functional impact of SLC2A11-MIF on bladder cancer cell proliferation, apoptosis, and metastasis.
  • To elucidate the molecular mechanisms underlying the oncogenic functions of SLC2A11-MIF.

Main Methods:

  • Analysis of The Cancer Genome Atlas and Sun Yat-Sen Memorial Hospital patient cohorts to identify SLC2A11-MIF upregulation.
  • In vitro and in vivo functional assays to assess the effects of SLC2A11-MIF on bladder cancer.
  • Co-immunoprecipitation and mRNA stability assays to determine the interaction of SLC2A11-MIF with PTBP1 and its downstream targets.
  • PTBP1 knockdown experiments to validate the role of the SLC2A11-MIF-PTBP1 axis.
  • Investigation of regulatory factors (CTCF, NATT10) and RNA modification (N4-acetylcytidine) in SLC2A11-MIF expression and stability.

Main Results:

  • The fusion transcript SLC2A11-MIF was identified and found to be upregulated in bladder cancer patient cohorts.
  • SLC2A11-MIF significantly enhanced bladder cancer cell proliferation, survival, and metastasis in vitro and in vivo.
  • The fusion protein encoded by SLC2A11-MIF interacts with PTBP1, regulating the mRNA stability of key oncogenes (e.g., PLK1, ROBO1, PIK3R3).
  • Knockdown of PTBP1 abrogated the pro-tumorigenic effects of SLC2A11-MIF.
  • SLC2A11-MIF expression is regulated by CTCF and stabilized by N4-acetylcytidine modification.

Conclusions:

  • The novel SLC2A11-MIF fusion transcript plays a significant role in bladder cancer progression.
  • The SLC2A11-MIF-PTBP1 axis is a critical regulator of mRNA stability and oncogenic functions in bladder cancer.
  • Understanding the regulatory mechanisms of SLC2A11-MIF offers potential therapeutic avenues for bladder cancer treatment.
Keywords:
PTBP1SLC2A11–MIFbladder cancerfusion proteinmRNA stabilitymetastasis

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