The role of prostate tumor overexpressed 1 in cancer progression

Verónica Cánovas _, Matilde Lleonart, Juan Morote and Rosanna Paciucci

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Oncotarget. 2017; 8:12451-12471. https://doi.org/10.18632/oncotarget.14104

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Verónica Cánovas1,4, Matilde Lleonart2,4, Juan Morote1,3,4, Rosanna Paciucci1,4

1Biomedical Research Group of Urology, Vall d’Hebron Research Institute, Pg. Vall d’Hebron 119-129, 08035 Barcelona, Spain

2Biomedical Research in Cancer Stem Cells, Vall d’Hebron Research Institute, Pg. Vall d’Hebron 119-129, 08035 Barcelona, Spain

3Deparment of Urology, Vall d’Hebron Hospital, Pg. Vall d’Hebron 119-129, 08035 Barcelona, Spain

4Universitat Autònoma de Barcelona, Spain

Correspondence to:

Rosanna Paciucci, email: [email protected]

Keywords: PTOV1, cancer progression, prostate cancer, cancer stem cells, transcription

Received: August 26, 2016     Accepted: November 14, 2016     Published: December 22, 2016


Prostate-Tumor-Overexpressed-1 (PTOV1) is a conserved adaptor protein discovered as overexpressed in prostate cancer. Since its discovery, the number of binding partners and associated cellular functions has increased and helped to identify PTOV1 as regulator of gene expression at transcription and translation levels. Its overexpression is associated with increased tumor grade and proliferation in prostate cancer and other neoplasms, including breast, ovarian, nasopharyngeal, squamous laryngeal, hepatocellular and urothelial carcinomas. An important contribution to higher levels of PTOV1 in prostate tumors is given by the frequent rate of gene amplifications, also found in other tumor types. The recent resolution of the structure by NMR of the PTOV domain in PTOV2, also identified as Arc92/ACID1/MED25, has helped to shed light on the functions of PTOV1 as a transcription factor. In parallel, by studying its interaction with RACK1, we have discovered PTOV1 action in promoting mRNAs translation. Here, we will focus on the role of PTOV1 in cancer, re-examine its pro-oncogenic effects and re-evaluate the most relevant interactions and evidences of its cellular functions. The data are used to formulate a model for the mechanisms of action of PTOV1 in line with its recently described activities and cellular pathways modulated in cancer.

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