Supplementary Figure 1 from Survival in Patients with High-Risk Prostate Cancer Is Predicted by miR-221, Which Regulates Proliferation, Apoptosis, and Invasion of Prostate Cancer Cells by Inhibiting IRF2 and SOCS3

Kneitz, Burkhard; Krebs, Markus; Kalogirou, Charis; Schubert, Maria; Joniau, Steven; van Poppel, Hein; Lerut, Evelyne; Kneitz, Susanne; Scholz, Claus Jürgen; Ströbel, Philipp; Gessler, Manfred; Riedmiller, Hubertus; Spahn, Martin

doi:10.1158/0008-5472.22401480.v1

Supplementary Figure 1 from Survival in Patients with High-Risk Prostate Cancer Is Predicted by miR-221, Which Regulates Proliferation, Apoptosis, and Invasion of Prostate Cancer Cells by Inhibiting IRF2 and SOCS3

journal contribution

posted on 2023-03-30, 22:27 authored by Burkhard Kneitz, Markus Krebs, Charis Kalogirou, Maria Schubert, Steven Joniau, Hein van Poppel, Evelyne Lerut, Susanne Kneitz, Claus Jürgen Scholz, Philipp Ströbel, Manfred Gessler, Hubertus Riedmiller, Martin Spahn

PDF file - 27K, Flow charts demonstrating the patient selection.

History

ARTICLE ABSTRACT

A lack of reliably informative biomarkers to distinguish indolent and lethal prostate cancer is one reason this disease is overtreated. miR-221 has been suggested as a biomarker in high-risk prostate cancer, but there is insufficient evidence of its potential utility. Here we report that miR-221 is an independent predictor for cancer-related death, extending and validating earlier findings. By mechanistic investigations we showed that miR-221 regulates cell growth, invasiveness, and apoptosis in prostate cancer at least partially via STAT1/STAT3-mediated activation of the JAK/STAT signaling pathway. miR-221 directly inhibits the expression of SOCS3 and IRF2, two oncogenes that negatively regulate this signaling pathway. miR-221 expression sensitized prostate cancer cells for IFN-γ–mediated growth inhibition. Our findings suggest that miR-221 offers a novel prognostic biomarker and therapeutic target in high-risk prostate cancer. Cancer Res; 74(9); 2591–603. ©2014 AACR.