Baicalein induces apoptosis in SCC-4 human tongue cancer cells via a Ca2+-dependent mitochondrial pathway

Yuh-Tzy Lin1, Jai-Sing Yang, Hui-Ju Lin

  • 1Department of Nursing and Management, Jen-Teh Junior College of Medicine, Taiwan, ROC.

In Vivo (Athens, Greece)
|January 24, 2008
PubMed
Abstract

Insights

Baicalein induces apoptosis in SCC-4 tongue cancer cells by activating the mitochondrial death pathway. This process involves calcium signaling and affects key apoptosis-related proteins, offering potential therapeutic insights.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Investigated the effects of baicalein on SCC-4 human tongue cancer cells.
  • Focused on understanding baicalein's impact on apoptosis and related signaling pathways in vitro.

Purpose of the Study:

  • To elucidate the mechanism of baicalein-induced apoptosis in SCC-4 cells.
  • To explore the role of calcium ions and mitochondrial pathways in this process.

Main Methods:

  • Utilized flow cytometry to analyze apoptosis, reactive oxygen species (ROS), cytoplasmic Ca2+, mitochondrial membrane potential (MMP), and caspase-3 activity.
  • Employed Western blotting to assess apoptosis-associated proteins including p53, BAX, BCL-2, cytochrome c, caspase-3, and caspase-9.

Main Results:

  • Baicalein treatment increased levels of p53, BAX, cytochrome c, caspase-3, and caspase-9, while decreasing BCL-2, indicating apoptosis induction.
  • Demonstrated cytochrome c release from mitochondria and caspase-3 activation, confirming apoptosis.
  • Showed that calcium chelation with BAPTA restored MMP, suppressed cytoplasmic Ca2+, and reduced apoptosis, highlighting a Ca2+-dependent pathway.

Conclusions:

  • Baicalein induces apoptotic cell death in SCC-4 cells.
  • Cellular calcium (Ca2+) plays a critical role in modulating baicalein-induced apoptosis through a mitochondrial pathway.
  • These findings suggest a potential therapeutic strategy targeting calcium signaling in tongue cancer treatment.