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Melanoma addiction to the long non-coding RNA SAMMSON

Eleonora Leucci, Roberto Vendramin, Marco Spinazzi, Patrick Laurette, Mark Fiers, Jasper Wouters, Enrico Radaelli, Sven Eyckerman (UGent) , Carina Leonelli (UGent) , Katrien Vanderheyden, et al.
(2016) NATURE. 531(7595). p.518-522
Author
Organization
Abstract
Focal amplifications of chromosome 3p13-3p14 occur in about 10% of melanomas and are associated with a poor prognosis. The melanoma-specific oncogene MITF resides at the epicentre of this amplicon(1). However, whether other loci present in this amplicon also contribute to melanomagenesis is unknown. Here we show that the recently annotated long non-coding RNA (lncRNA) gene SAMMSON is consistently co-gained with MITF. In addition, SAMMSON is a target of the lineage-specific transcription factor SOX10 and its expression is detectable in more than 90% of human melanomas. Whereas exogenous SAMMSON increases the clonogenic potential in trans, SAMMSON knockdown drastically decreases the viability of melanoma cells irrespective of their transcriptional cell state and BRAF, NRAS or TP53 mutational status. Moreover, SAMMSON targeting sensitizes melanoma to MAPK-targeting therapeutics both in vitro and in patient-derived xenograft models. Mechanistically, SAMMSON interacts with p32, a master regulator of mitochondrial homeostasis and metabolism, to increase its mitochondrial targeting and pro-oncogenic function. Our results indicate that silencing of the lineage addiction oncogene SAMMSON disrupts vital mitochondrial functions in a cancer-cell-specific manner; this silencing is therefore expected to deliver highly effective and tissue-restricted anti-melanoma therapeutic responses.
Keywords
TARGET, SURVIVAL, P32/GC1QR, MITOCHONDRIAL TRANSLATION, P-32 PROTEIN, OXIDATIVE-PHOSPHORYLATION, METABOLISM, PROLIFERATION, MORPHOLOGY, PGC1-ALPHA

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MLA
Leucci, Eleonora, et al. “Melanoma Addiction to the Long Non-Coding RNA SAMMSON.” NATURE, vol. 531, no. 7595, 2016, pp. 518–22, doi:10.1038/nature17161.
APA
Leucci, E., Vendramin, R., Spinazzi, M., Laurette, P., Fiers, M., Wouters, J., … Marine, J.-C. (2016). Melanoma addiction to the long non-coding RNA SAMMSON. NATURE, 531(7595), 518–522. https://doi.org/10.1038/nature17161
Chicago author-date
Leucci, Eleonora, Roberto Vendramin, Marco Spinazzi, Patrick Laurette, Mark Fiers, Jasper Wouters, Enrico Radaelli, et al. 2016. “Melanoma Addiction to the Long Non-Coding RNA SAMMSON.” NATURE 531 (7595): 518–22. https://doi.org/10.1038/nature17161.
Chicago author-date (all authors)
Leucci, Eleonora, Roberto Vendramin, Marco Spinazzi, Patrick Laurette, Mark Fiers, Jasper Wouters, Enrico Radaelli, Sven Eyckerman, Carina Leonelli, Katrien Vanderheyden, Aljosja Rogiers, Els Hermans, Pieter Baatsen, Stein Aerts, Frederic Amant, Stefan Van Aelst, Joost van den Oord, Bart de Strooper, Irwin Davidson, Denis LJ Lafontaine, Kris Gevaert, Jo Vandesompele, Pieter Mestdagh, and Jean-Christophe Marine. 2016. “Melanoma Addiction to the Long Non-Coding RNA SAMMSON.” NATURE 531 (7595): 518–522. doi:10.1038/nature17161.
Vancouver
1.
Leucci E, Vendramin R, Spinazzi M, Laurette P, Fiers M, Wouters J, et al. Melanoma addiction to the long non-coding RNA SAMMSON. NATURE. 2016;531(7595):518–22.
IEEE
[1]
E. Leucci et al., “Melanoma addiction to the long non-coding RNA SAMMSON,” NATURE, vol. 531, no. 7595, pp. 518–522, 2016.
@article{7222564,
  abstract     = {{Focal amplifications of chromosome 3p13-3p14 occur in about 10% of melanomas and are associated with a poor prognosis. The melanoma-specific oncogene MITF resides at the epicentre of this amplicon(1). However, whether other loci present in this amplicon also contribute to melanomagenesis is unknown. Here we show that the recently annotated long non-coding RNA (lncRNA) gene SAMMSON is consistently co-gained with MITF. In addition, SAMMSON is a target of the lineage-specific transcription factor SOX10 and its expression is detectable in more than 90% of human melanomas. Whereas exogenous SAMMSON increases the clonogenic potential in trans, SAMMSON knockdown drastically decreases the viability of melanoma cells irrespective of their transcriptional cell state and BRAF, NRAS or TP53 mutational status. Moreover, SAMMSON targeting sensitizes melanoma to MAPK-targeting therapeutics both in vitro and in patient-derived xenograft models. Mechanistically, SAMMSON interacts with p32, a master regulator of mitochondrial homeostasis and metabolism, to increase its mitochondrial targeting and pro-oncogenic function. Our results indicate that silencing of the lineage addiction oncogene SAMMSON disrupts vital mitochondrial functions in a cancer-cell-specific manner; this silencing is therefore expected to deliver highly effective and tissue-restricted anti-melanoma therapeutic responses.}},
  author       = {{Leucci, Eleonora and Vendramin, Roberto and Spinazzi, Marco and Laurette, Patrick and Fiers, Mark and Wouters, Jasper and Radaelli, Enrico and Eyckerman, Sven and Leonelli, Carina and Vanderheyden, Katrien and Rogiers, Aljosja and Hermans, Els and Baatsen, Pieter and Aerts, Stein and Amant, Frederic and Van Aelst, Stefan and van den Oord, Joost and de Strooper, Bart and Davidson, Irwin and Lafontaine, Denis LJ and Gevaert, Kris and Vandesompele, Jo and Mestdagh, Pieter and Marine, Jean-Christophe}},
  issn         = {{0028-0836}},
  journal      = {{NATURE}},
  keywords     = {{TARGET,SURVIVAL,P32/GC1QR,MITOCHONDRIAL TRANSLATION,P-32 PROTEIN,OXIDATIVE-PHOSPHORYLATION,METABOLISM,PROLIFERATION,MORPHOLOGY,PGC1-ALPHA}},
  language     = {{eng}},
  number       = {{7595}},
  pages        = {{518--522}},
  title        = {{Melanoma addiction to the long non-coding RNA SAMMSON}},
  url          = {{http://doi.org/10.1038/nature17161}},
  volume       = {{531}},
  year         = {{2016}},
}
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