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. 2016 Sep;18(9):1006-17.
doi: 10.1038/ncb3399. Epub 2016 Aug 22.

Melanoma miRNA trafficking controls tumour primary niche formation

Shani Dror  1 , Laureen Sander  2 , Hila Schwartz  3 , Danna Sheinboim  1 , Aviv Barzilai  4 , Yuval Dishon  1 , Sebastien Apcher  5 , Tamar Golan  1 , Shoshana Greenberger  4 , Iris Barshack  4 , Hagar Malcov  1 , Alona Zilberberg  1 , Lotan Levin  1 , Michelle Nessling  6 , Yael Friedmann  7 , Vivien Igras  8 , Ohad Barzilay  9 , Hananya Vaknine  10 , Ronen Brenner  10 , Assaf Zinger  11 , Avi Schroeder  11 , Pinchas Gonen  1 , Mehdi Khaled  12 , Neta Erez  3 , Jörg D Hoheisel  2 , Carmit Levy  1
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Melanoma miRNA trafficking controls tumour primary niche formation

Shani Dror (V体育安卓版) et al. Nat Cell Biol. 2016 Sep.

VSports最新版本 - Abstract

Melanoma originates in the epidermis and becomes metastatic after invasion into the dermis. Prior interactions between melanoma cells and dermis are poorly studied. Here, we show that melanoma cells directly affect the formation of the dermal tumour niche by microRNA trafficking before invasion. Melanocytes, cells of melanoma origin, are specialized in releasing pigment vesicles, termed melanosomes. In melanoma in situ, we found melanosome markers in distal fibroblasts before melanoma invasion VSports手机版. The melanosomes carry microRNAs into primary fibroblasts triggering changes, including increased proliferation, migration and pro-inflammatory gene expression, all known features of cancer-associated fibroblasts (CAFs). Specifically, melanosomal microRNA-211 directly targets IGF2R and leads to MAPK signalling activation, which reciprocally encourages melanoma growth. Melanosome release inhibitor prevented CAF formation. Since the first interaction of melanoma cells with blood vessels occurs in the dermis, our data suggest an opportunity to block melanoma invasion by preventing the formation of the dermal tumour niche. .

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