Epigenetic Silencing of CDR1as Drives IGF2BP3-Mediated Melanoma Invasion and Metastasis.
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Epigenetic Silencing of CDR1as Drives IGF2BP3-Mediated Melanoma Invasion and Metastasis.

Hanniford, Douglas;Ulloa-Morales, Alejandro;Karz, Alcida;Berzoti-Coelho, Maria Gabriela;Moubarak, Rana S;Sánchez-Sendra, Beatriz;Kloetgen, Andreas;Davalos, Veronica;Imig, Jochen;Wu, Pamela;Vasudevaraja, Varshini;Argibay, Diana;Lilja, Karin;Tabaglio, Tommaso;Monteagudo, Carlos;Guccione, Ernesto;Tsirigos, Aristotelis;Osman, Iman;Aifantis, Iannis;Hernando, Eva;
cancer cell 2020 Vol. 37 pp. 55-70.e15
266
hanniford2020epigeneticcancer

Abstract

Metastasis is the primary cause of death of cancer patients. Dissecting mechanisms governing metastatic spread may uncover important tumor biology and/or yield promising therapeutic insights. Here, we investigated the role of circular RNAs (circRNA) in metastasis, using melanoma as a model aggressive tumor. We identified silencing of cerebellar degeneration-related 1 antisense (CDR1as), a regulator of miR-7, as a hallmark of melanoma progression. CDR1as depletion results from epigenetic silencing of LINC00632, its originating long non-coding RNA (lncRNA) and promotes invasion in vitro and metastasis in vivo through a miR-7-independent, IGF2BP3-mediated mechanism. Moreover, CDR1as levels reflect cellular states associated with distinct therapeutic responses. Our study reveals functional, prognostic, and predictive roles for CDR1as and expose circRNAs as key players in metastasis.

Keywords

melanoma metastasis gpx4 prc2 cdr1as ezh2 igf2bp linc00632 circrna mir-7

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