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Microenvironmental control of malignancy exerted by RNASET2, a widely conserved extracellular RNase

Francesco Acquati1, Sabrina Bertilaccio, Annalisa Grimaldi

  • 1Dipartimento di Biotecnologie e Scienze Molecolari, Faculty of Medicine, Università degli Studi dell'Insubria, 21100 Varese, Italy.

Proceedings of the National Academy of Sciences of the United States of America
|December 30, 2010
PubMed

Insights

The human RNASET2 gene, a tumor antagonizing/malignancy suppressor gene (TAG/MSG), controls ovarian tumorigenesis in vivo by modulating the tumor microenvironment and immune cells, despite lacking in vitro activity.

Area of Science:

  • Oncology
  • Molecular Biology
  • Immunology

Background:

  • Stromal cells play a critical role in regulating neoplasia progression.
  • Tumor antagonizing/malignancy suppressor genes (TAG/MSG) are emerging as key regulators of stromal-epithelial interactions in cancer.
  • RNASET2, an extracellular RNase, is downregulated in ovarian tumors and melanoma.

Purpose of the Study:

  • To functionally characterize the human RNASET2 gene's role in ovarian tumorigenesis.
  • To investigate the in vivo mechanisms by which RNASET2 suppresses tumors.
  • To determine if RNASET2 fits the definition of a tumor-antagonizing gene.

Main Methods:

  • Functional characterization of human RNASET2.
  • In vivo studies of ovarian tumorigenesis.
  • Analysis of the tumor microenvironment and immune cell infiltration.
  • In vitro assays to assess RNASET2 activity.

Main Results:

  • RNASET2 exhibited no detectable activity in standard in vitro assays.
  • Significant control of ovarian tumorigenesis was observed in vivo.
  • RNASET2 mediated tumor suppression through microenvironment modification.
  • Induction of monocyte/macrophage lineage immune cells was observed.

Conclusions:

  • RNASET2 functions as a tumor suppressor gene in ovarian cancer.
  • Its tumor-antagonizing activity is mediated by in vivo microenvironmental and immune modulation.
  • RNASET2 represents a novel member of the tumor-antagonizing gene family.

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