Related Experiment Video

Updated: Nov 20, 2025

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
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Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

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Neferine induces p38 MAPK/JNK1/2 activation to modulate melanoma proliferation, apoptosis, and oxidative stress

Jun Xie1, Ming-Hui Chen1, Chuan-Peng Ying1

  • 1Institute of Dermatology and Venereology, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, Chengdu, China.

Annals of Translational Medicine
|January 25, 2021
PubMed
Abstract

Insights

Neferine, a natural compound, effectively inhibits melanoma cell proliferation and invasion while promoting apoptosis. This study demonstrates its potential as an effective treatment for melanoma by targeting key signaling pathways.

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Melanoma is an aggressive skin cancer with limited treatment options for advanced stages.
  • Investigating novel therapeutic agents is crucial for improving patient outcomes.

Purpose of the Study:

  • To evaluate the antitumor effects of neferine in melanoma.
  • To elucidate the underlying molecular mechanisms of neferine's action.

Main Methods:

  • In vitro studies using A375 and C32 melanoma cell lines.
  • In vivo xenograft mouse model to assess therapeutic efficacy.
  • Assays included proliferation, invasion, apoptosis, mitochondrial function, reactive oxygen species (ROS) generation, and Western blot analysis for signaling pathway activation.

Main Results:

  • Neferine significantly inhibited melanoma cell proliferation and invasion, and induced apoptosis in vitro.
  • Neferine treatment led to mitochondrial dysfunction, increased ROS and MDA levels, and decreased SOD levels.
  • In vivo, neferine suppressed tumor growth, reduced Ki67 and survivin expression, and activated p38 and JNK1/2 phosphorylation.

Conclusions:

  • Neferine exhibits potent antitumor activity against melanoma.
  • Its mechanism involves inducing apoptosis, disrupting mitochondrial function, and modulating ROS levels.
  • Neferine's therapeutic potential is likely mediated through the activation of p38 and JNK signaling pathways.
Keywords:
DNA replicationNeferineapoptosismelanomatumorigenesis

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