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ASPL-TFE3 Oncoprotein Regulates Cell Cycle Progression and Induces Cellular Senescence by Up-Regulating p21.

Naoko Ishiguro1, Haruhiko Yoshida2

  • 1Department of Pathobiological Science and Technology, Faculty of Medicine, Tottori University, 86 Nishimachi, Yonago, Tottori 683-8503, Japan.

Neoplasia (New York, N.Y.)
|September 28, 2016
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Alveolar soft part sarcoma (ASPS) tumorigenesis involves the ASPL-TFE3 fusion oncogene, which drives cell cycle arrest and senescence by upregulating p21. This process may promote tumor growth via the senescence-associated secretory phenotype (SASP).

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Alveolar soft part sarcoma (ASPS) is a rare soft tissue sarcoma with a poor prognosis.
  • The ASPL-TFE3 fusion gene, resulting from a chromosomal translocation, is a key driver in ASPS tumorigenesis.
  • The precise molecular mechanisms by which ASPL-TFE3 contributes to tumor development are not fully understood.

Purpose of the Study:

  • To identify direct transcriptional targets of the ASPL-TFE3 oncoprotein.
  • To elucidate the role of ASPL-TFE3 in cell cycle regulation and cellular senescence.
  • To investigate the potential contribution of ASPL-TFE3-induced senescence to the tumor microenvironment.

Main Methods:

  • Ectopic expression of ASPL-TFE3 in 293 cells and human bone marrow-derived mesenchymal stem cells.
  • Analysis of p21 (CDKN1A) protein and mRNA levels.
  • Chromatin immunoprecipitation and reporter assays to assess transcriptional activity on the p21 promoter.
  • Measurement of senescence-associated β-galactosidase activity and proinflammatory cytokine production.

Main Results:

  • p21 was identified as a direct transcriptional target of ASPL-TFE3.
  • ASPL-TFE3 expression led to cell cycle arrest and increased p21 levels in a p53-independent manner.
  • ASPL-TFE3 induced cellular senescence and upregulated proinflammatory cytokines associated with the senescence-associated secretory phenotype (SASP).
  • Suppression of p21 abrogated ASPL-TFE3-mediated cellular senescence.

Conclusions:

  • ASPL-TFE3 oncogene induces cellular senescence by directly upregulating p21 expression.
  • ASPL-TFE3-induced senescence may promote tumorigenesis through the induction of SASP, potentially creating a protumorigenic microenvironment.
  • Targeting the ASPL-TFE3/p21 pathway could offer therapeutic strategies for ASPS.