Shikonin-induced Apoptosis of Colon Cancer Cells Is Reduced by Peroxiredoxin V Expression

Nisansala Chandimali1, Hu-Nan Sun2, Ling-Zu Kong1

  • 1Interdisciplinary Graduate Program in Advanced Convergence Technology and Science, Jeju National University, Jeju, Republic of Korea.

Anticancer Research
|November 10, 2019
PubMed
Abstract

Insights

Shikonin induces colon cancer cell death by regulating mTOR signaling. Overexpressing peroxiredoxin V (PrxV) blocks this effect, suggesting PrxV as a potential therapeutic target for colon cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Natural Product Chemistry

Background:

  • Colon cancer is a leading cause of cancer-related mortality worldwide.
  • Natural plant extracts, like Shikonin, show promise as anti-cancer agents.
  • Understanding Shikonin's mechanisms in colon cancer is crucial for improved treatment.

Purpose of the Study:

  • To investigate the effects of Shikonin on colon cancer cell apoptosis.
  • To explore the role of peroxiredoxin V (PrxV) in Shikonin-induced apoptosis.

Main Methods:

  • In vitro experiments using a colon cancer cell line.
  • Construction of a colon cancer cell line overexpressing PrxV.
  • Analysis of Shikonin's impact on apoptosis and mTOR signaling.

Main Results:

  • Shikonin effectively induced apoptosis in colon cancer cells.
  • Shikonin's pro-apoptotic effect was mediated through the mammalian target of rapamycin (mTOR) signaling pathway.
  • Overexpression of PrxV significantly inhibited Shikonin-induced apoptosis.

Conclusions:

  • Shikonin demonstrates potential as a therapeutic agent for colon cancer by inducing apoptosis.
  • Targeting PrxV may represent a novel strategy to enhance Shikonin's efficacy in colon cancer treatment.