Supplementary Methods, Figures 1-6 from The Adaptor Protein AMOT Promotes the Proliferation of Mammary Epithelial Cells via the Prolonged Activation of the Extracellular Signal-Regulated Kinases

Ranahan, William P.; Han, Zhang; Smith-Kinnaman, Whitney; Nabinger, Sarah C.; Heller, Brigitte; Herbert, Britney-Shea; Chan, Rebecca; Wells, Clark D.

doi:10.1158/0008-5472.22386383.v1

00085472can101995-sup-can_10-1995_ranahan_methods_f6.pdf (1.37 MB)

Supplementary Methods, Figures 1-6 from The Adaptor Protein AMOT Promotes the Proliferation of Mammary Epithelial Cells via the Prolonged Activation of the Extracellular Signal-Regulated Kinases

journal contribution

posted on 2023-03-30, 20:06 authored by William P. Ranahan, Zhang Han, Whitney Smith-Kinnaman, Sarah C. Nabinger, Brigitte Heller, Britney-Shea Herbert, Rebecca Chan, Clark D. Wells

Supplementary Methods, Figures 1-6 from The Adaptor Protein AMOT Promotes the Proliferation of Mammary Epithelial Cells via the Prolonged Activation of the Extracellular Signal-Regulated Kinases

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ARTICLE ABSTRACT

The asymmetric organization of epithelial cells is a basic counter to cellular proliferation. However, the mechanisms whereby pro-growth pathways are modulated by intracellular factors that control cell shape are not well understood. This study demonstrates that the adaptor protein Amot, in addition to its established role in regulating cellular asymmetry, also promotes extracellular signal-regulated kinase 1 and 2 (ERK1/2)–dependent proliferation of mammary cells. Specifically, expression of Amot80, but not a mutant lacking its polarity protein interaction domain, enhances ERK1/2-dependent proliferation of MCF7 cells. Further, expression of Amot80 induces nontransformed MCF10A cells to overgrow as disorganized cellular aggregates in Matrigel. Conversely, Amot expression is required for proliferation of breast cancer cells in specific microenvironmental contexts that require ERK1/2 signaling. Thus, Amot is proposed to coordinate the dysregulation of cell polarity with the induction of neoplastic growth in mammary cells. Cancer Res; 71(6); 2203–11. ©2011 AACR.