American Association for Cancer Research
00085472can161589-sup-166620_1_supp_3739668_qghjfz.doc (35 kB)

Supplementary Figure Legend from RB Loss Promotes Prostate Cancer Metastasis

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posted on 2023-03-31, 01:05 authored by Chellappagounder Thangavel, Ettickan Boopathi, Yi Liu, Alex Haber, Adam Ertel, Anshul Bhardwaj, Sankar Addya, Noelle Williams, Stephen J. Ciment, Paolo Cotzia, Jeffry L. Dean, Adam Snook, Chris McNair, Matt Price, James R. Hernandez, Shuang G. Zhao, Ruth Birbe, James B. McCarthy, Eva A. Turley, Kenneth J. Pienta, Felix Y. Feng, Adam P. Dicker, Karen E. Knudsen, Robert B. Den

Supplementary Figure Legends Supplemental Figure S1. RB loss promotes cell migration and invasion. Supplemental Figure S2. RB regulates RHAMM expression. Supplemental Figure S3. RB/E2F Binds on the RHAMM Promoter. Supplemental Figure S4. RHAMM overexpression drives cancer cell migration, invasion, and EMT. Supplemental Figure S5. RHAMM Inhibition Diminishes Migration and Invasion, but not Cellular Proliferation.


Prostate Cancer Foundation

American Cancer Society




RB loss occurs commonly in neoplasia but its contributions to advanced cancer have not been assessed directly. Here we show that RB loss in multiple murine models of cancer produces a prometastatic phenotype. Gene expression analyses showed that regulation of the cell motility receptor RHAMM by the RB/E2F pathway was critical for epithelial–mesenchymal transition, motility, and invasion by cancer cells. Genetic modulation or pharmacologic inhibition of RHAMM activity was sufficient and necessary for metastatic phenotypes induced by RB loss in prostate cancer. Mechanistic studies in this setting established that RHAMM stabilized F-actin polymerization by controlling ROCK signaling. Collectively, our findings show how RB loss drives metastatic capacity and highlight RHAMM as a candidate therapeutic target for treating advanced prostate cancer. Cancer Res; 77(4); 982–95. ©2016 AACR.