First published March 1, 2017 - More info
We investigated whether TGF-β induced by anticancer therapies accelerates tumor progression. Using the MMTV/PyVmT transgenic model of metastatic breast cancer, we show that administration of ionizing radiation or doxorubicin caused increased circulating levels of TGF-β1 as well as increased circulating tumor cells and lung metastases. These effects were abrogated by administration of a neutralizing pan–TGF-β antibody. Circulating polyomavirus middle T antigen–expressing tumor cells did not grow ex vivo in the presence of the TGF-β antibody, suggesting autocrine TGF-β is a survival signal in these cells. Radiation failed to enhance lung metastases in mice bearing tumors that lack the type II TGF-β receptor, suggesting that the increase in metastases was due, at least in part, to a direct effect of TGF-β on the cancer cells. These data implicate TGF-β induced by anticancer therapy as a prometastatic signal in tumor cells and provide a rationale for the simultaneous use of these therapies in combination with TGF-β inhibitors.
Swati Biswas, Marta Guix, Cammie Rinehart, Teresa C. Dugger, Anna Chytil, Harold L. Moses, Michael L. Freeman, Carlos L. Arteaga
Original citation: J Clin Invest. 2007;117(5):1305–1313. https://doi.org/10.1172/JCI30740
Citation for this corrigendum: J Clin Invest. 2017;127(3):1116. https://doi.org/10.1172/JCI93333
The editors recently became aware that the images for control and irradiated samples for PyVmT/TGFBR2KO mice in Figure 6B are from the same section. The authors were able to provide original source data from a replicate experiment. The corrected panel appears below.
The authors regret the error.