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Cancer proteome and metabolite changes linked to SHMT2
Jiefei Tong1, Jonathan R Krieger2, Paul Taylor1,2
1Program in Cell Biology, The Hospital for Sick Children, Toronto, Canada.
Plos One
|September 9, 2020
Summary
Serine hydroxymethyltransferase 2 (SHMT2) overexpression boosts cancer cell growth. SHMT2 knockdown causes glycine auxotrophy and impacts mitochondrial respiration, revealing its role in cancer metabolism.
Area of Science:
- Biochemistry
- Cancer Biology
- Metabolomics
Background:
- Serine hydroxymethyltransferase 2 (SHMT2) is upregulated in various cancers.
- SHMT2 plays a key role in folate and one-carbon metabolism.
Purpose of the Study:
- To investigate the role of SHMT2 in cancer cell proliferation and metabolism.
- To elucidate the molecular mechanisms linking SHMT2 to cancer progression.
Main Methods:
- Utilized HeLa cells with inducible SHMT2 overexpression or knockdown.
- Analyzed cell proliferation, metabolite levels, and proteome.
- Employed proximity biotinylation (BioID) to identify SHMT2-interacting proteins.
Main Results:
- SHMT2 overexpression enhanced cell proliferation and tumor growth.
- SHMT2 knockdown led to glycine auxotrophy and AICAR accumulation.
- SHMT2 levels inversely correlated with mitochondrial respiration complex proteins.
- Identified 48 mitochondrial proteins associated with SHMT2, including ACOT2 and GLUD1.
Conclusions:
- SHMT2 overexpression promotes cancer growth.
- SHMT2 influences glycine metabolism and purine synthesis.
- SHMT2 interacts with mitochondrial proteins, impacting cellular respiration and potentially cancer metabolism.
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