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SIRT3 Overexpression Inhibits Growth of Kidney Tumor Cells and Enhances Mitochondrial Biogenesis

Huan Liu1, Siying Li2, Xiaohui Liu1

  • 1MOE Key Laboratory of Bioinformatics, Center for Synthetic and Systematic Biology, School of Life Sciences , Tsinghua University , Beijing 100084 , China.

Journal of Proteome Research
|August 11, 2018
PubMed

Insights

Sirtuin 3 (SIRT3) protein deacetylase activity impacts kidney cancer growth by regulating mitochondrial function. SIRT3 downregulation promotes the Warburg effect in clear cell renal cell carcinoma (ccRCC).

Area of Science:

  • Mitochondrial biology
  • Cancer metabolism
  • Renal cell carcinoma research

Background:

  • Sirtuin 3 (SIRT3), a NAD+-dependent mitochondrial deacetylase, is crucial for metabolism and mitochondrial health.
  • SIRT3 is downregulated in clear cell renal cell carcinoma (ccRCC), the most common kidney cancer.
  • The role of SIRT3 in ccRCC tumorigenesis, despite the cancer's known metabolic and mitochondrial alterations, remains unclear.

Purpose of the Study:

  • To investigate the role of SIRT3 in ccRCC tumorigenesis and development.
  • To determine SIRT3's impact on ccRCC cell proliferation, mitochondrial mass, and oxidative stress.
  • To elucidate the molecular mechanisms by which SIRT3 influences ccRCC metabolism and mitochondrial biogenesis.

Main Methods:

  • SIRT3 overexpression and knockdown in ccRCC cell lines.
  • Cell proliferation assays, mitochondrial mass quantification, and reactive oxygen species (ROS) level measurements.
  • Metabolomics, quantitative proteomics, and TFAM (transcription factor A, mitochondrial) deacetylation and interaction studies.

Main Results:

  • SIRT3 overexpression decreased ccRCC cell proliferation and increased mitochondrial mass.
  • SIRT3 overexpression elevated ROS levels and sensitized cells to oxidative stress.
  • SIRT3 reversed the Warburg effect in ccRCC cells, promoting mitochondrial biogenesis via TFAM deacetylation and enhancing its DNA binding.

Conclusions:

  • SIRT3 plays a significant role in regulating mitochondrial biogenesis in ccRCC.
  • Downregulation of SIRT3 promotes a Warburg phenotype, contributing to ccRCC development.
  • Targeting SIRT3 may offer a therapeutic strategy for ccRCC by restoring mitochondrial function.
Keywords:
SIRT3TFAMclear cell renal cell carcinomadeacetylationmitochondrial biogenesisproteomics

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