Restoration of wild-type PTEN expression leads to apoptosis, induces differentiation, and reduces telomerase activity in human glioma cells

Xin Xia Tian, Jesse C.S. Pang, Shing Shun Tony To, Ho Keung Ng

Research output: Journal article publicationJournal articleAcademic researchpeer-review

49 Citations (Scopus)

Abstract

PTEN is a candidate tumor suppressor gene identified on human chromosome 10q23.3 that is frequently mutated or deleted in 30% to 44% of glioblastomas. Transient expression study of PTEN in glioma cells indicates that PTEN plays an important role in cellular proliferation, tumorigenicity, cell migration, and focal adhesions. In this study, we examined the biological consequences on U87MG glioma cells after stable gene transfer of wild-type PTEN. Cells stably expressing wild-type PTEN protein were found to have suppressed proliferation, as determined by cell counting and Ki-67 staining, as well as inhibited anchorage-independent growth. The PTEN-expressing cells also showed higher expression of glial fibrillary acidic protein and changed morphologically from spindle-shaped to elongated cell bodies with multiple slender processes, suggesting that these cells have undergone differentiation. In addition, telomerase activity decreased more than 10- fold in PTEN-expressing cells when compared with control cells. More importantly, apoptosis was detected in about 5% of PTEN-expressing cells, representing a 17-fold (p < 0.01) increase over the control cells. Taken together, these results suggest that PTEN plays an important role in regulation of cell homeostasis by maintaining a balance between proliferation, differentiation, and apoptosis.
Original languageEnglish
Pages (from-to)472-479
Number of pages8
JournalJournal of Neuropathology and Experimental Neurology
Volume58
Issue number5
DOIs
Publication statusPublished - 1 Jan 1999

Keywords

  • Apoptosis
  • Differentiation
  • Glioma
  • Proliferation
  • PTEN
  • Telomerase

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Neurology
  • Clinical Neurology
  • Cellular and Molecular Neuroscience

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