[The role of non-coding RNAs in the pathogenesis of multiple endocrine neoplasia syndrome type 1]

Elizaveta O Mamedova1, Diana A Dimitrova1, Zhanna E Belaya1

  • 1Endocrinology Research Centre.

Problemy Endokrinologii
|December 22, 2020
PubMed

Insights

Non-coding RNAs (ncRNAs) may influence tumor development in Multiple Endocrine Neoplasia syndrome type 1 (MEN1). Understanding menin protein interactions with ncRNAs could reveal new therapeutic targets for MEN1 and related tumors.

Area of Science:

  • Endocrinology
  • Oncology
  • Molecular Biology

Background:

  • Multiple Endocrine Neoplasia syndrome type 1 (MEN1) is a rare genetic disorder linked to MEN1 gene mutations and menin protein.
  • MEN1 is associated with various endocrine and non-endocrine tumors, but its exact pathogenesis remains unclear.
  • Phenocopies of MEN1, lacking MEN1 gene mutations, present similar clinical features with unknown causes.

Purpose of the Study:

  • To explore the potential role of non-coding ribonucleic acids (ncRNAs) in the pathogenesis of MEN1-associated tumors.
  • To investigate how altered ncRNA expression might influence signaling pathways involving the menin protein.
  • To identify potential therapeutic targets by understanding menin-ncRNA interactions in MEN1 and its phenocopies.

Main Methods:

  • Review of existing literature on ncRNA expression in endocrine tumors.
  • Analysis of signaling pathways regulated by the menin protein.
  • Comparative study of gene expression profiles in MEN1 patients and phenocopies (hypothetical, based on abstract).

Main Results:

  • Changes in ncRNA expression are implicated in the development of various tumors.
  • Altered ncRNAs may dysregulate signaling pathways involving menin, contributing to MEN1 tumor formation.
  • Identifying menin-interacting agents is crucial for understanding MEN1 pathogenesis.

Conclusions:

  • ncRNAs represent a potential contributing factor to MEN1 tumorigenesis and its phenocopies.
  • Further research into menin-ncRNA interactions is warranted for therapeutic advancements in MEN1.
  • Understanding these molecular mechanisms can improve knowledge of tumor development in MEN1 syndrome.

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