ROR1 contributes to melanoma cell growth and migration by regulating N-cadherin expression via the PI3K/Akt pathway.

摘要: The Receptor tyrosine kinase-like Orphan 1 (ROR1) is primarily expressed by neural crest cells during embryogenesis. Following a complete downregulation after birth, ROR1 was shown to re-express in various types of cancers. Little known about expression and function melanoma. Here we show that aberrantly both melanoma cell lines tumors its associates with poor Post-Recurrence Survival Using gain- loss-of-function approaches found enhances anchorage-dependent -independent growth cells. In addition, decreases adhesion increases motility migration. Mechanistically, induce upregulation Akt the mesenquimal markers N-cadherin vimentin. regulation relies on dependent independent mechanisms. does not affect Wnt canonical pathway but be engaged positive feedback loop Wnt5a. summary, contributes progression candidate biomarker prognosis. Although further studies are needed confirm this possibility, present work indicates good prospective target for cancer therapy. © 2015 Wiley Periodicals, Inc.