ArticleNature2016
Melanoma addiction to the long non-coding RNA SAMMSON.
Article in Nature, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 353 papers.
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Who cites it
353 citing papers in PubMed, 583 citations in OpenAlex.
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- LncRNA-protein interactions: molecular switches for the precise regulation of innate immunity.Frontiers in immunology · 2026Review
- Insight into the emerging role of long non-coding RNAs in BRAF inhibitor resistance in melanoma.Frontiers in oncology · 2026Review
- Epigenetics of Malignant Melanoma: Mechanisms, Diagnostic Approaches and Therapeutic Applications.Oncology research · 2026Review
- Integrated transcriptome and single-cell sequencing analysis identify blood-pancreas shared lncRNA biomarkers in new-onset T2DM.PloS one · 2026Article
- Mitochondria-specific targeting of noncanonicalTheranostics · 2026Article
- Identification of Long Noncoding RNA by In Situ Hybridization Approaches.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Long non-coding RNAs in glioblastoma: from molecular drivers to therapeutic targets.Frontiers in immunology · 2026Review
- Interaction of lncRNA LENT with DHX36 regulates translation and suppresses autophagy in melanoma.Cell death & disease · 2025Article
293 more citing papers are in PubMed but not listed here.
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Authors and funding
24 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
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. 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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.