Harmine hydrochloride induces G0/G1 cell cycle arrest and apoptosis in oral squamous carcinoma cells

Weiting Lin1, Yizhen Li2, Hsinyi Huang2

  • 1Department of Stomatology, Ditmanson Medical Foundation Chiayi Christian Hospital, Chiayi 600, Taiwan, R.O.C.

Insights

Harmine hydrochloride (HH) shows anticancer effects against oral squamous cell carcinoma (OSCC). This compound induces cell cycle arrest and apoptosis, suggesting its potential as a novel therapeutic agent for oral cancer.

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Oral squamous cell carcinoma (OSCC) has a poor 5-year survival rate, necessitating novel therapeutic strategies.
  • Harmine, a β-carboline alkaloid, exhibits anticancer properties.
  • Harmine hydrochloride (HH), a more soluble and stable derivative, is a promising candidate for cancer treatment.

Purpose of the Study:

  • To investigate the anticancer activity of harmine hydrochloride (HH) in oral squamous cell carcinoma (OSCC) cells.
  • To elucidate the mechanisms underlying HH's cytotoxic effects, including cell cycle and apoptosis.
  • To identify signaling pathways modulated by HH in OSCC.

Main Methods:

  • Cytotoxicity was assessed using the Cell Counting Kit-8 assay in OSCC cell lines (SCC-4, SCC-25).
  • Cell cycle progression and apoptosis were analyzed via flow cytometry.
  • Protein expression and signaling pathway involvement were examined using Western blotting and a pan-caspase inhibitor (Z-VAD-FMK).

Main Results:

  • Harmine hydrochloride (HH) demonstrated significant cytotoxic effects against OSCC cells.
  • HH treatment induced G0/G1 phase cell cycle arrest and apoptosis in OSCC cells.
  • The MAPK signaling pathway was implicated in HH-induced apoptosis in SCC-4 cells.

Conclusions:

  • Harmine hydrochloride (HH) possesses notable anticancer activity against oral squamous cell carcinoma.
  • HH induces cell cycle arrest and apoptosis, highlighting its therapeutic potential.
  • HH may serve as a future therapeutic agent for oral cancer treatment, particularly involving the MAPK pathway.