Neferine induces apoptosis by modulating the ROS‑mediated JNK pathway in esophageal squamous cell carcinoma

Kang An1, Yuehan Zhang1, Yingjiao Liu1

  • 1Department of Gastroenterology, Hebei General Hospital, Shijiazhuang, Hebei 050051, P.R. China.

Oncology Reports
|July 25, 2020
PubMed

Insights

Neferine, a natural compound, shows promise in treating esophageal squamous cell carcinoma (ESCC). It inhibits cancer cell growth by activating the ROS-JNK pathway and inhibiting Nrf2.

Area of Science:

  • Oncology
  • Pharmacology
  • Biochemistry

Background:

  • Esophageal squamous cell carcinoma (ESCC) treatments have limited efficacy.
  • Novel therapeutic targets are crucial for improving patient survival rates.
  • Neferine, a natural product from Nelumbo nucifera, inhibits various cancer cells but its effect on ESCC is unknown.

Purpose of the Study:

  • To investigate the anti-cancer effects of neferine on ESCC.
  • To elucidate the underlying molecular mechanisms of neferine's action in ESCC.

Main Methods:

  • Assessing neferine's anti-proliferative effects on ESCC cell lines.
  • Analyzing cell cycle progression (G2/M arrest) and apoptosis induction.
  • Measuring reactive oxygen species (ROS) generation and JNK pathway activation.
  • Investigating the role of N-acetyl cysteine (NAC) as a ROS inhibitor.
  • Examining the impact of neferine on Nrf2 expression.

Main Results:

  • Neferine demonstrated significant anti-proliferative effects on ESCC cells.
  • Neferine induced G2/M phase arrest and enhanced apoptosis.
  • Neferine triggered ROS accumulation and activated the JNK pathway.
  • ROS and JNK inhibition reversed neferine-induced cell cycle arrest and apoptosis.
  • Neferine inhibited the antioxidant factor Nrf2.

Conclusions:

  • Neferine exhibits antitumor effects against ESCC.
  • The mechanism involves ROS-mediated JNK pathway activation and Nrf2 inhibition.
  • Neferine shows potential as a novel therapeutic agent for ESCC.

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