The Rb tumor suppressor regulates epithelial cell migration and polarity
Author(s)Parisi, Tiziana; Balsamo, Michele; Gertler, Frank; Lees, Jacqueline
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Altered cell polarity and migration are hallmarks of cancer and metastases. Here we show that inactivation of the retinoblastoma gene (Rb) tumor suppressor causes defects in tissue closure that reflect the inability of Rb null epithelial cells to efficiently migrate and polarize. These defects occur independently of pRB's anti-proliferative role and instead correlate with upregulation of RhoA signaling and mislocalization of apical-basal polarity proteins. Notably, concomitant inactivation of tp53 specifically overrides the motility defect, and not the aberrant polarity, thereby uncovering previously unappreciated mechanisms by which Rb and tp53 mutations cooperate to promote cancer development and metastases. Keywords: aPKC; eyes open phenotype; PAR complex; planar cell polarity; RhoA Rock signaling
DepartmentDavid H. Koch Institute for Integrative Cancer Research at MIT; Massachusetts Institute of Technology. Department of Biology
Parisi, Tiziana et al., "The Rb tumor suppressor regulates epithelial cell migration and polarity." Molecular Carcinogenesis 57, 11 (November 2018): 1640–1650. © 2018 Wiley Periodicals, Inc.
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