Triptolide inhibits pituitary adenoma cell viability, migration and invasion via ADAM12/EGFR signaling pathway

Junwen Wang1, Zhuo Zhang1, Ran Li1

  • 1Sino-German Neuro-Oncology Molecular Laboratory, Department of Neurosurgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.

Life Sciences
|December 31, 2017
PubMed
Abstract

Insights

Triptolide effectively inhibits pituitary adenoma cell growth, migration, and invasion by targeting the ADAM12/EGFR pathway. This natural compound shows promise for treating pituitary adenomas.

Area of Science:

  • Endocrinology
  • Oncology
  • Molecular Biology

Background:

  • Triptolide from Tripterygium wilfordii exhibits broad-spectrum antitumor activity.
  • The role of triptolide in pituitary adenomas is currently unknown.

Purpose of the Study:

  • To investigate the effect of triptolide on pituitary adenoma cell viability, migration, and invasion.
  • To elucidate the underlying molecular mechanism involving ADAM12/EGFR signaling.

Main Methods:

  • Mouse pituitary adenoma cell lines (TtT/GF and AtT20) were treated with varying triptolide concentrations.
  • Assessed effects on cell viability, migration, invasion, and apoptosis.
  • Investigated the role of ADAM12 (a disintegrin and metalloprotease 12)/EGFR signaling.

Main Results:

  • Triptolide significantly inhibited cell viability, migration, and invasion in a dose-dependent manner.
  • Triptolide reduced ADAM12 expression and attenuated ADAM12/EGFR signaling.
  • Triptolide suppressed pituitary adenoma cell tumorigenesis in vivo.

Conclusions:

  • Triptolide inhibits pituitary adenoma progression through the ADAM12/EGFR pathway.
  • Triptolide demonstrates potential as a therapeutic agent for pituitary adenomas.

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