Telomerase reactivation following telomere dysfunction yields murine prostate tumors with bone metastases

Zhihu Ding, Chang Jiun Wu, Mariela Jaskelioff, Elena Ivanova, Maria Kost-Alimova, Alexei Protopopov, Gerald C. Chu, Guocan Wang, Xin Lu, Emma S. Labrot, Jian Hu, Wei Wang, Yonghong Xiao, Hailei Zhang, Jianhua Zhang, Jingfang Zhang, Boyi Gan, Samuel R. Perry, Shan Jiang, Liren LiJames W. Horner, Y. Alan Wang, Lynda Chin, Ronald A. Depinho

Research output: Contribution to journalArticlepeer-review

179 Scopus citations

Abstract

To determine the role of telomere dysfunction and telomerase reactivation in generating pro-oncogenic genomic events and in carcinoma progression, an inducible telomerase reverse transcriptase (mTert) allele was crossed onto a prostate cancer-prone mouse model null for Pten and p53 tumor suppressors. Constitutive telomerase deficiency and associated telomere dysfunction constrained cancer progression. In contrast, telomerase reactivation in the setting of telomere dysfunction alleviated intratumoral DNA-damage signaling and generated aggressive cancers with rearranged genomes and new tumor biological properties (bone metastases). Comparative oncogenomic analysis revealed numerous recurrent amplifications and deletions of relevance to human prostate cancer. Murine tumors show enrichment of the TGF-β/SMAD4 network, and genetic validation studies confirmed the cooperative roles of Pten, p53, and Smad4 deficiencies in prostate cancer progression, including skeletal metastases. Thus, telomerase reactivation in tumor cells experiencing telomere dysfunction enables full malignant progression and provides a mechanism for acquisition of cancer-relevant genomic events endowing new tumor biological capabilities.

Original languageEnglish (US)
Pages (from-to)896-907
Number of pages12
JournalCell
Volume148
Issue number5
DOIs
StatePublished - Mar 2 2012

ASJC Scopus subject areas

  • General Biochemistry, Genetics and Molecular Biology

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