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Epithelial-mesenchymal transition can suppress major attributes of human epithelial tumor-initiating cells
Toni Celià-Terrassa, … , Pedro L. Fernández, Timothy M. Thomson
Toni Celià-Terrassa, … , Pedro L. Fernández, Timothy M. Thomson
Published April 16, 2012
Citation Information: J Clin Invest. 2012;122(5):1849-1868. https://doi.org/10.1172/JCI59218.
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Research Article Oncology

Epithelial-mesenchymal transition can suppress major attributes of human epithelial tumor-initiating cells

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Abstract

Malignant progression in cancer requires populations of tumor-initiating cells (TICs) endowed with unlimited self renewal, survival under stress, and establishment of distant metastases. Additionally, the acquisition of invasive properties driven by epithelial-mesenchymal transition (EMT) is critical for the evolution of neoplastic cells into fully metastatic populations. Here, we characterize 2 human cellular models derived from prostate and bladder cancer cell lines to better understand the relationship between TIC and EMT programs in local invasiveness and distant metastasis. The model tumor subpopulations that expressed a strong epithelial gene program were enriched in highly metastatic TICs, while a second subpopulation with stable mesenchymal traits was impoverished in TICs. Constitutive overexpression of the transcription factor Snai1 in the epithelial/TIC-enriched populations engaged a mesenchymal gene program and suppressed their self renewal and metastatic phenotypes. Conversely, knockdown of EMT factors in the mesenchymal-like prostate cancer cell subpopulation caused a gain in epithelial features and properties of TICs. Both tumor cell subpopulations cooperated so that the nonmetastatic mesenchymal-like prostate cancer subpopulation enhanced the in vitro invasiveness of the metastatic epithelial subpopulation and, in vivo, promoted the escape of the latter from primary implantation sites and accelerated their metastatic colonization. Our models provide new insights into how dynamic interactions among epithelial, self-renewal, and mesenchymal gene programs determine the plasticity of epithelial TICs.

Authors

Toni Celià-Terrassa, Óscar Meca-Cortés, Francesca Mateo, Alexia Martínez de Paz, Nuria Rubio, Anna Arnal-Estapé, Brian J. Ell, Raquel Bermudo, Alba Díaz, Marta Guerra-Rebollo, Juan José Lozano, Conchi Estarás, Catalina Ulloa, Daniel ρlvarez-Simón, Jordi Milà, Ramón Vilella, Rosanna Paciucci, Marian Martínez-Balbás, Antonio García de Herreros, Roger R. Gomis, Yibin Kang, Jerónimo Blanco, Pedro L. Fernández, Timothy M. Thomson

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Figure 11

PC-3/S cells facilitate the spread and metastatic growth of PC-3/Mc cells.

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PC-3/S cells facilitate the spread and metastatic growth of PC-3/Mc
    ...
(A) Orthotopic coimplantation of GFP-PC-3/Mc cells with RFP- and Renilla luciferase–expressing PC-3/S cells in the ventral prostate of NOD-SCID mice diminished their growth rate at the implantation, while accelerating the appearance of metastatic growth. Bioluminescence monitoring was performed separately for the anterior and posterior halves of the mice, for improved resolution. Middle: growth curves of orthotopically implanted tumor cells, with photon counts normalized relative to values on day 0. Right: Kaplan-Meier actuarial plots for metastasis-free mice. (B) Coimplantation (i.m.) of GFP-PC-3/Mc cells with RFP-PC-3/S cells diminished their growth rate as compared with GFP-PC-3/Mc cells implanted alone. Bottom: graphical representation of growth at the implantation site. (C) Coinoculation (i.v.) of GFP-PC-3/Mc cells with RFP-PC-3/S cells accelerated their lung colonization. Bottom: Kaplan-Meier actuarial plots for lung colony–free mice. (D) Coinoculation (i.c.) of GFP-PC-3/Mc cells with RFP-PC-3/S cells did not significantly affect their bone colonization efficiency. Right panel: Kaplan-Meier actuarial plots for bone colony–free mice. Results are expressed as mean ± SEM.

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ISSN: 0021-9738 (print), 1558-8238 (online)

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