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The serine hydroxymethyltransferase-2 (SHMT2) initiates lymphoma development through epigenetic tumor suppressor

Sara Parsa1, Ana Ortega-Molina1, Hsia-Yuan Ying2

  • 1Cancer Biology and Genetics, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.

Nature Cancer
|February 11, 2021
PubMed

Insights

Amplification of serine hydroxymethyltransferase-2 (SHMT2) cooperates with BCL2 to initiate lymphoma. SHMT2 promotes epigenetic silencing of tumor suppressors, driving lymphomagenesis.

Area of Science:

  • Oncology
  • Cancer Metabolism
  • Epigenetics

Background:

  • Cancer cells exhibit altered metabolism for growth.
  • Metabolic enzyme activity is rarely considered a primary driver of cancer.
  • The role of serine hydroxymethyltransferase-2 (SHMT2) in lymphoma initiation is unexplored.

Purpose of the Study:

  • To investigate the role of SHMT2 in lymphoma initiation.
  • To understand the mechanism by which SHMT2 contributes to lymphomagenesis.

Main Methods:

  • Analysis of SHMT2 localization to chromosome 12q14.1 in lymphoma.
  • Investigating the cooperation between SHMT2 and BCL2 in lymphoma development.
  • Assessing the impact of SHMT2 loss or inhibition on lymphoma cell survival.
  • Examining SHMT2's role in DNA and histone methylation patterns.

Main Results:

  • SHMT2 is located at chromosome 12q14.1, a region with frequent copy number gains in lymphoma.
  • Elevated SHMT2 expression collaborates with BCL2 to promote lymphoma.
  • SHMT2 inhibition or loss reduces lymphoma cell survival.
  • SHMT2 alters DNA and histone methylation, silencing tumor suppressor genes like SASH1 and PTPRM.

Conclusions:

  • SHMT2 amplification, in conjunction with BCL2, is sufficient for initiating lymphomagenesis.
  • SHMT2 drives lymphoma initiation by epigenetically silencing tumor suppressor genes.

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