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USP22 down-regulation facilitates human retinoblastoma cell aging and apoptosis via inhibiting TERT/P53 pathway

D Zhou1, P Liu, D-W Sun

  • 1Department of Eye Hospital, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China. shaominpeng18@163.com.

European Review for Medical and Pharmacological Sciences
|July 7, 2017
PubMed
Abstract

Insights

USP22 promotes retinoblastoma cell growth by maintaining telomerase activity and inhibiting cell aging. Reducing USP22 expression induces retinoblastoma cell aging and apoptosis via the TERT/P53 pathway, suggesting USP22 as a potential therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Retinoblastoma is a common childhood intraocular malignancy with limited treatment options.
  • Tumor cell immortality is linked to elevated telomerase activity, a potential therapeutic target.
  • USP22's role in retinoblastoma cell immortality and aging via the TERT/P53 pathway requires elucidation.

Purpose of the Study:

  • To investigate the role of USP22 in retinoblastoma cell proliferation, immortality, aging, and apoptosis.
  • To explore the involvement of the TERT/P53 signaling pathway in USP22's effects on retinoblastoma cells.

Main Methods:

  • Cell proliferation assessed by MTT assay.
  • Protein and mRNA levels of USP22, TERT, and P53 measured by Western blot and RT-qPCR.
  • Telomerase activity detected by TRAP assay.
  • Apoptosis and DNA damage quantified by flow cytometry and comet assay.
  • Cell aging evaluated by β-galactosidase staining.

Main Results:

  • USP22 overexpression increased retinoblastoma cell proliferation and telomerase activity while elevating TERT and reducing P53 expression.
  • Overexpression of USP22 inhibited cell aging, apoptosis, and DNA damage.
  • Down-regulation of USP22 produced opposite effects, promoting aging and apoptosis.

Conclusions:

  • USP22 significantly influences retinoblastoma cell proliferation, aging, and apoptosis.
  • Decreased USP22 expression induces retinoblastoma cell aging and apoptosis by suppressing the TERT/P53 pathway.
  • USP22 represents a potential therapeutic target for retinoblastoma treatment.

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