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Aldolase B attenuates clear cell renal cell carcinoma progression by inhibiting CtBP2

Mingyue Tan1,2, Qi Pan1, Qi Wu1,3

  • 1Department of Urology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200080, China.

Frontiers of Medicine
|February 15, 2023
PubMed

Insights

Aldolase B (ALDOB) inhibits clear cell renal cell carcinoma (ccRCC) progression by interacting with CtBP2. This interaction, independent of ALDOB’s enzymatic activity, reduces tumor growth and metastasis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Aldolase B (ALDOB) is depleted in clear cell renal cell carcinoma (ccRCC).
  • Previous studies indicated ALDOB inhibits ccRCC proliferation via a non-enzymatic mechanism, but the precise pathway remained unclear.
  • Identifying novel protein interactions of ALDOB is crucial for understanding its role in ccRCC pathogenesis.

Purpose of the Study:

  • To elucidate the mechanism by which ALDOB inhibits ccRCC proliferation and metastasis.
  • To identify novel ALDOB-interacting proteins in ccRCC.
  • To investigate the functional consequences of the ALDOB-CtBP2 interaction in ccRCC progression.

Main Methods:

  • Co-immunoprecipitation to identify ALDOB-interacting proteins.
  • Analysis of clinical ccRCC samples to correlate protein expression ratios with patient survival and gene expression.
  • Cell-based assays to assess the impact of ALDOB-CtBP2 interaction on cell proliferation, migration, and gene expression.
  • Xenograft and metastasis models to evaluate tumor growth and metastatic potential in vivo.

Main Results:

  • C-terminal-binding protein 2 (CtBP2) was identified as a novel ALDOB-interacting protein in ccRCC.
  • A higher CtBP2-to-ALDOB expression ratio in ccRCC tissues correlated with increased expression of CtBP2 target genes and poorer patient survival.
  • ALDOB inhibited CtBP2-mediated gene repression, leading to decreased proliferation and migration of ccRCC cells in an ALDOB-CtBP2 interaction-dependent manner.
  • ALDOB acted as a scaffold, recruiting acireductone dioxygenase 1 to CtBP2, thereby enhancing the inhibition of CtBP2 activity via 4-methylthio 2-oxobutyric acid.
  • Overexpression of ALDOB suppressed tumor growth and reduced lung metastasis in vivo.

Conclusions:

  • ALDOB functions as a tumor suppressor in ccRCC by negatively regulating CtBP2 activity through a non-enzymatic scaffolding mechanism.
  • The ALDOB-CtBP2 interaction pathway represents a potential therapeutic target for inhibiting ccRCC growth and metastasis.
Keywords:
ALDOBcell proliferationkidney cancer

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