Nintedanib induces apoptosis in human pterygium cells through the FGFR2-ERK signalling pathway

Yan Gong1, Yan-Hong Liao1, Quan-Yong Yi1

  • 1Ningbo Eye Hospital, Ningbo 315042, Zhejiang Province, China.

Abstract

Insights

Nintedanib inhibits pterygium cell growth by inducing apoptosis. This occurs through the fibroblast growth factor receptor 2 (FGFR2)/extracellular-signal-regulated kinase (ERK) pathway, offering a potential therapeutic target.

Area of Science:

  • Ophthalmology
  • Cell Biology
  • Pharmacology

Background:

  • Pterygium is a proliferative eye condition.
  • The fibroblast growth factor receptor 2 (FGFR2)/extracellular-signal-regulated kinase (ERK) pathway is implicated in cell growth.

Purpose of the Study:

  • To investigate if nintedanib inhibits pterygium cells.
  • To determine if this inhibition involves the FGFR2/ERK pathway.

Main Methods:

  • In vitro culture of human primary pterygium cells.
  • Treatment with nintedanib, followed by morphological and apoptosis analysis.
  • Western blot for apoptosis-related proteins and molecular docking for nintedanib-FGFR2 binding.

Main Results:

  • Nintedanib inhibited pterygium cell growth and induced apoptosis.
  • Increased Bax and cleaved-Caspase3, decreased Bcl-2 expression observed.
  • Nintedanib inhibited ERK1/2 phosphorylation via FGFR2, which was abolished by FGFR2 silencing.

Conclusions:

  • Nintedanib induces apoptosis in pterygium cells.
  • The mechanism involves the inhibition of the FGFR2/ERK pathway.

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