Vernodalin Triggers ROS-Mediated Apoptosis in TPC-1 Human PapillaryThyroid Cancer Cells via Suppression of the MAPKs

Xijia Yang1, Meng Wei2, Yuan An3

  • 1Department of General Surgery, Xi'an Gaoxin Hospital, Xi'an, 710000, China.

Abstract

Insights

Vernodalin (VN) effectively inhibits human papillary thyroid cancer (PTC) cell growth by inducing cell death through increased reactive oxygen species (ROS) and apoptosis. This sesquiterpene shows promise as a potential chemotherapy agent for thyroid cancer.

Area of Science:

  • Endocrinology
  • Oncology
  • Pharmacology

Background:

  • Thyroid cancer (TC) incidence is rising globally.
  • Vernodalin (VN), a sesquiterpene, shows anticancer activity in breast and liver cells.
  • VN's effects on human papillary thyroid cancer (PTC) remain unexplored.

Purpose of the Study:

  • To investigate the antitumor and antiproliferative effects of Vernodalin (VN) on human PTC cells.
  • To elucidate the apoptosis mechanisms induced by VN in TPC-1 cells.

Main Methods:

  • Cell viability assessed via MTT assay.
  • Reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) measured using specific staining methods.
  • Apoptosis visualized through AO/EB and DAPI staining; MAPK pathway markers analyzed by western blotting.

Main Results:

  • VN inhibited PTC cell growth in a concentration-dependent manner.
  • VN treatment increased intracellular ROS and damaged MMP, inducing apoptosis.
  • VN-induced TPC-1 cell death occurred via ROS generation and the MAPK signaling pathway.

Conclusions:

  • VN demonstrates potential as an apoptosis-inducing agent in PTC.
  • VN may be a valuable therapeutic agent in human PTC chemotherapy.
  • Further in vivo studies using animal models are warranted to confirm VN's anti-cancer efficacy.

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