Related Experiment Video

Updated: Nov 11, 2025

Endoscopic Endonasal Trans-sphenoidal Approach: Minimally Invasive Surgery for Pituitary Adenomas
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Endoscopic Endonasal Trans-sphenoidal Approach: Minimally Invasive Surgery for Pituitary Adenomas

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NEK2 regulates cellular proliferation and cabergoline sensitivity in pituitary adenomas

Fangfang Jian1,2, Yuhao Sun2, Qingfang Sun2

  • 1Department of Obstetrics and Gynecology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Journal of Cancer
|March 23, 2021
PubMed

Insights

NEK2 is upregulated in prolactinomas, driving tumor growth and resistance to dopamine agonist treatment. Targeting NEK2 offers a potential therapeutic strategy for prolactinoma.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Oncology

Background:

  • Prolactinomas are pituitary tumors often treated with dopamine agonists (DAs).
  • Dopamine resistance is a clinical challenge in prolactinoma management.
  • The molecular mechanisms underlying prolactinoma progression and DA resistance require further elucidation.

Purpose of the Study:

  • To investigate the role of NEK2 in prolactinoma development and progression.
  • To explore the underlying mechanisms of NEK2's function in prolactinomas.
  • To assess NEK2 as a potential therapeutic target for prolactinoma.

Main Methods:

  • RNA sequencing of MMQ cells treated with cabergoline (CAB).
  • Quantitative real-time PCR, western immunoblotting, and immunohistochemistry to assess NEK2 expression in pituitary adenomas.
  • Gain-of-function and loss-of-function assays to evaluate NEK2's role in cell proliferation.
  • Co-immunoprecipitation to study NEK2-USP7 interaction.

Main Results:

  • NEK2 expression is upregulated in prolactinomas, especially in dopamine-resistant cases.
  • NEK2 overexpression enhances pituitary tumor cell proliferation and reduces sensitivity to CAB.
  • NEK2 knockdown inhibits cell growth and increases sensitivity to CAB.
  • NEK2 regulates cell proliferation via the Wnt signaling pathway.
  • USP7 interacts with, deubiquitylates, and stabilizes NEK2.

Conclusions:

  • NEK2 plays a critical role in prolactinoma cell proliferation and dopamine agonist resistance.
  • The NEK2-USP7 interaction is a key mechanism in regulating NEK2 stability.
  • NEK2 represents a promising therapeutic target for prolactinoma treatment.
Keywords:
NEK2USP7cabergoline sensitivityprolactinoma

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