Format

Send to

Choose Destination
Life Sci. 2018 Feb 1;194:150-156. doi: 10.1016/j.lfs.2017.12.037. Epub 2017 Dec 27.

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

Author information

1
Sino-German Neuro-Oncology Molecular Laboratory, Department of Neurosurgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
2
Sino-German Neuro-Oncology Molecular Laboratory, Department of Neurosurgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China. Electronic address: Kshu@tjh.tjmu.edu.cn.
3
Sino-German Neuro-Oncology Molecular Laboratory, Department of Neurosurgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China. Electronic address: tlei@tjh.tjmu.edu.cn.

Abstract

AIM:

Triptolide, an effective component derived from Tripterygium wilfordii, has been well recognized to process a broad-spectrum antitumor activities in various tumor types. However, the potential role of triptolide in pituitary adenomas remains unknown. The aim of this study was to investigate the precise role of triptolide and underlying mechanism in regulating pituitary adenoma cell viability, migration and invasion.

MAIN METHODS:

We use mouse pituitary adenoma cells (TtT/GF and AtT20 cells) as the experiment model and treated them with varying concentrations of triptolide. The corresponding inhibitory effects on cell viability, migration, invasion and apoptosis were examined respectively, and the underlying mechanism was determined by investigating ADAM12 (a disintegrin and metalloprotease 12)/EGFR signaling.

KEY FINDINGS:

Triptolide significantly inhibited cell viability, migration and invasion in TtT/GF and AtT20 cells in a dose-dependent manner. Mechanistically, triptolide significantly reduced ADAM12 expression at protein levels and attenuated ADAM12/EGFR signaling. Meanwhile, triptolide treatment combined with ADAM12 silencing enhanced the suppression effects on cell viability, migration and invasion, and those effects were restored following ADAM12-rescued. Moreover, triptolide suppressed the tumorigenesis of TtT/GF and AtT20 cells in vivo.

SIGNIFICANCE:

Our research provides evidence that triptolide inhibits pituitary adenoma cell viability, migration and invasion via ADAM12/EGFR signaling pathway. These findings suggest a potential role for triptolide in treating pituitary adenomas.

KEYWORDS:

ADAM12; EGFR; Pituitary adenomas; Triptolide

PMID:
29288766
DOI:
10.1016/j.lfs.2017.12.037
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center