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MicroRNA-93 mediates cabergoline resistance by targeting ATG7 in prolactinoma

Zerui Wu1, Lin Cai2, Jianglong Lu3

  • 1Z Wu, Neurosurgery, First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.

The Journal of Endocrinology
|November 4, 2018
PubMed

Insights

MicroRNA-93 (miRNA-93) drives resistance to dopamine agonist (DA) therapy in prolactinomas by inhibiting autophagy via targeting ATG7. Downregulating miRNA-93 may restore DA sensitivity and promote tumor cell death.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Oncology

Background:

  • Dopamine agonist (DA)-resistant prolactinomas present a significant clinical challenge.
  • Increased microRNA-93 (miRNA-93) expression was previously observed in DA-resistant prolactinomas, but its role is unclear.

Purpose of the Study:

  • To investigate the role of miRNA-93 in mediating resistance to cabergoline (CAB) in prolactinoma cells.
  • To explore the impact of miRNA-93 on cellular autophagy and its relationship with autophagy-related 7 (ATG7).

Main Methods:

  • Bioinformatic analysis to identify miRNA-93 targets.
  • In vitro studies using MMQ and GH3 cells with miRNA-93 overexpression or inhibition.
  • Analysis of autophagy markers and cell viability.
  • Protein expression analysis and luciferase assays to confirm miRNA-93 and ATG7 interaction.
  • In vivo xenograft models in nude mice.

Main Results:

  • miRNA-93 expression was elevated, and ATG7 expression was downregulated in DA-resistant prolactinomas.
  • miRNA-93 overexpression reduced CAB's cytotoxic effect, while miRNA-93 inhibition enhanced CAB efficacy and induced apoptosis via autophagy.
  • ATG7 overexpression reversed the resistance induced by miRNA-93.
  • Findings were validated in vivo.

Conclusions:

  • miRNA-93 contributes to cabergoline resistance in prolactinomas by downregulating autophagy through targeting ATG7.
  • miRNA-93 represents a potential therapeutic target for overcoming DA resistance in prolactinoma treatment.

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