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lncRNA - Long Non-coding RNAs02:39

lncRNA - Long Non-coding RNAs

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In humans, more than 80% of the genome gets transcribed. However, only around 2% of the genome codes for proteins. The remaining part produces non-coding RNAs which includes ribosomal RNAs, transfer RNAs, telomerase RNAs, and regulatory RNAs, among other types. A large number of regulatory non-coding RNAs have been classified into two groups depending upon their length – small non-coding RNAs, such as microRNA, which are less than 200 nucleotides in length, and long non-coding RNA...
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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
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Melanoma addiction to the long non-coding RNA SAMMSON.

Eleonora Leucci1,2, Roberto Vendramin1,2, Marco Spinazzi2

  • 1Laboratory For Molecular Cancer Biology, Center for Human Genetics, KULeuven, Herestraat 49, 3000 Leuven, Belgium.

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Summary

The long non-coding RNA SAMMSON is a melanoma oncogene co-amplified with MITF. Targeting SAMMSON disrupts mitochondrial function and enhances melanoma therapy response.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Focal amplifications at chromosome 3p13-3p14 are found in ~10% of melanomas, correlating with poor prognosis.
  • The melanoma-specific oncogene MITF is located at the center of this amplicon, but the roles of other co-amplified genes remain unclear.

Purpose of the Study:

  • To investigate the role of the long non-coding RNA (lncRNA) gene SAMMSON, located within the 3p13-3p14 amplicon, in melanoma development and therapeutic response.

Main Methods:

  • Analysis of SAMMSON co-amplification with MITF in melanoma.
  • Assessing SAMMSON expression in melanoma cells and patient samples.
  • Investigating the functional impact of SAMMSON modulation (overexpression and knockdown) on melanoma cell viability and clonogenicity.
  • Evaluating the effect of SAMMSON targeting on melanoma sensitivity to MAPK inhibitors in vitro and in vivo.
  • Elucidating the molecular mechanism of SAMMSON action, including its interaction with p32 and mitochondrial function.

Main Results:

  • SAMMSON is consistently co-gained with MITF in 3p13-3p14 amplifications and is a SOX10 target, expressed in over 90% of melanomas.
  • SAMMSON overexpression enhances melanoma cell clonogenicity, while its knockdown severely impairs cell viability across different melanoma subtypes.
  • Targeting SAMMSON sensitizes melanoma cells to MAPK-targeting therapies in vitro and in patient-derived xenografts.
  • SAMMSON interacts with p32, promoting its mitochondrial localization and pro-oncogenic activity, thereby disrupting mitochondrial homeostasis.

Conclusions:

  • SAMMSON acts as a lineage addiction oncogene in melanoma.
  • Silencing SAMMSON disrupts essential mitochondrial functions in a cancer-specific manner.
  • Targeting SAMMSON holds promise for developing effective and tissue-restricted anti-melanoma therapies.