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Isocitrate dehydrogenase 3β (IDH3β) regulates the cell cycle and TCA cycle in esophageal squamous cell carcinoma (ESCC). IDH3β overexpression promotes cancer cell proliferation and correlates with poor patient survival.

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Area of Science:

  • Cell Biology
  • Metabolic Regulation
  • Cancer Research

Background:

  • Metabolic activities and cell-cycle progression are linked, but specific molecular connections are not fully understood.
  • Esophageal squamous cell carcinoma (ESCC) is a significant health concern with complex underlying molecular mechanisms.

Purpose of the Study:

  • To identify novel regulators connecting metabolic pathways and cell-cycle progression in ESCC.
  • To investigate the role of isocitrate dehydrogenase 3β (IDH3β) in ESCC cell-cycle regulation and proliferation.

Main Methods:

  • Identification of IDH3β as a substrate of the anaphase-promoting complex/cyclosome (APC/C)-CDH1.
  • Analysis of IDH3β expression and its impact on cell-cycle transition (G1-S) in ESCC cells.
  • Assessment of α-ketoglutarate (α-KG) levels and PFKFB3 protein expression.
  • In vitro and in vivo proliferation assays.
  • Correlation analysis with patient survival data.

Main Results:

  • IDH3β was identified as a novel APC/C-CDH1 substrate and regulator of the cell cycle.
  • IDH3β is upregulated in late G1 phase in ESCC, accelerating G1-S transition and promoting proliferation.
  • IDH3β levels influence α-KG metabolite and PFKFB3 protein expression, impacting glucose uptake.
  • High IDH3β expression is linked to poorer survival in ESCC patients.

Conclusions:

  • IDH3β acts as a crucial link between the tricarboxylic acid (TCA) cycle and cell-cycle progression in ESCC.
  • IDH3β's cell-cycle-dependent expression and role in promoting proliferation suggest its potential as a prognostic marker and therapeutic target in ESCC.