Abstract:
:Melanoma cells use different migratory strategies to exit the primary tumor mass and invade surrounding and subsequently distant tissues. We reported previously that ADAR1 expression is downregulated in metastatic melanoma, thereby facilitating proliferation. Here we show that ADAR1 silencing enhances melanoma cell invasiveness and ITGB3 expression. The enhanced invasion is reversed when ITGB3 is blocked with antibodies. Re-expression of wild-type or catalytically inactive ADAR1 establishes this mechanism as independent of RNA editing. We demonstrate that ADAR1 controls ITGB3 expression both at the post-transcriptional and transcriptional levels, via miR-22 and PAX6 transcription factor, respectively. These are proven here as direct regulators of ITGB3 expression. miR-22 expression is controlled by ADAR1 via FOXD1 transcription factor. Clinical relevance is demonstrated in patient-paired progression tissue microarray using immunohistochemistry. The novel ADAR1-dependent and RNA-editing-independent regulation of invasion, mediated by ITGB3, strongly points to a central involvement of ADAR1 in cancer progression and metastasis.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Nemlich Y,Baruch EN,Besser MJ,Shoshan E,Bar-Eli M,Anafi L,Barshack I,Schachter J,Ortenberg R,Markel Gdoi
10.1038/s41467-018-04600-2subject
Has Abstractpub_date
2018-05-31 00:00:00pages
2154issue
1issn
2041-1723pii
10.1038/s41467-018-04600-2journal_volume
9pub_type
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