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Molecular characterization of epithelial-mesenchymal transition and medical treatment related-genes in

Joan Gil1,2,3, Montserrat Marques-Pamies1,4, Elena Valassi1,2,3

  • 1Endocrine Research Unit, Germans Trias i Pujol Research Institute (IGTP), Badalona, Spain.

Frontiers in Endocrinology
|April 10, 2023
PubMed
Abstract

Insights

Non-functioning pituitary neuroendocrine tumors (NF-PitNET) exhibit increased epithelial-mesenchymal transition (EMT), impacting treatment response. PEBP1 may predict tumor recurrence, while SSTR3 targeting shows therapeutic potential, excluding silent corticotroph adenomas.

Area of Science:

  • Endocrinology
  • Oncology
  • Molecular Biology

Background:

  • Non-functioning pituitary neuroendocrine tumors (NF-PitNET) are often resistant to medical therapies.
  • Epithelial-mesenchymal transition (EMT) is implicated in treatment resistance across various cancers, including pituitary adenomas.

Purpose of the Study:

  • To investigate the expression of EMT markers in NF-PitNET.
  • To assess somatostatin receptors and dopamine-associated genes for potential therapeutic strategies in NF-PitNET.

Main Methods:

  • Analysis of EMT markers and receptor/gene expression in 72 NF-PitNET and 16 non-tumoral pituitaries.
  • Comparison of EMT prevalence between NF-PitNET and GH-secreting pituitary tumors.

Main Results:

  • EMT markers (SNAI1, SNAI2, Vimentin, KLK10, PEBP1, Ki-67) and SSTR2 were associated with invasive NF-PitNET.
  • EMT was more prevalent in NF-PitNET than in GH-secreting tumors.
  • PEBP1 overexpression correlated with recurrent NF-PitNET, showing high sensitivity for predicting regrowth.
  • SSTR3 was highly expressed in NF-PitNET, but heterogeneously, with low levels in silent corticotroph adenomas.

Conclusions:

  • NF-PitNET demonstrates an enhanced EMT phenomenon.
  • SSTR3 targeting is a potential therapeutic approach for most NF-PitNET, except silent corticotroph adenomas.
  • PEBP1 serves as a valuable biomarker for predicting NF-PitNET regrowth.
Keywords:
Epithelial-mesenchymal transitiondopamine agonistsnon-functioning pituitary adenomassomatostatin analogssomatostatin receptor ligands

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