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Fisetin effects on cell proliferation and apoptosis in glioma cells

Fulya Pak1, Pinar Oztopcu-Vatan2

  • 1Graduated School of Natural and Applied Sciences, Eskisehir Osmangazi University, Eskisehir, Turkey.

Zeitschrift Fur Naturforschung. C, Journal of Biosciences
|August 18, 2019
PubMed

Insights

Fisetin exhibits significant antiproliferative and apoptotic effects on T98G glioma cells, showing greater efficacy than carmustine. This natural compound demonstrates potential as an alternative glioma treatment.

Area of Science:

  • Pharmacology and Toxicology
  • Cell Biology
  • Cancer Research

Background:

  • Glioblastoma multiforme (GBM) remains a challenging malignancy with limited treatment options.
  • Natural compounds are being explored for their potential anticancer properties.
  • Fisetin, a flavonoid, has shown promise in preclinical studies, but its specific effects on glioma cells require further elucidation.

Purpose of the Study:

  • To investigate the antiproliferative and cytotoxic effects of fisetin on T98G (glioblastoma) and BEAS-2B (normal bronchial epithelial) cells.
  • To compare the apoptotic and necrotic effects of fisetin in these cell lines.
  • To evaluate the potential of fisetin as an alternative therapeutic agent for gliomas.

Main Methods:

  • Cell viability was assessed using the MTT assay to determine the half-maximal inhibitory concentration (IC50) of fisetin.
  • Apoptotic alterations in fisetin-treated T98G cells were visualized using transmission electron microscopy.
  • Expression levels of apoptosis-related proteins (CASPASE 3, 9, 8, BAX, BCL-2, survivin) were analyzed in T98G cells.

Main Results:

  • Fisetin demonstrated dose- and time-dependent antiproliferative effects in both T98G and BEAS-2B cells.
  • The IC50 values for fisetin were significantly lower in T98G cells (75-93 μM) compared to BEAS-2B cells (90-270 μM) at 48 hours.
  • Fisetin induced apoptosis more effectively in T98G cells than in BEAS-2B cells, with increased expression of pro-apoptotic proteins (CASPASEs, BAX) and decreased expression of anti-apoptotic proteins (BCL-2, survivin).

Conclusions:

  • Fisetin exhibits potent dose- and time-dependent antiproliferative and apoptotic effects, particularly in T98G glioma cells.
  • Fisetin's cytotoxicity is more pronounced in T98G cells compared to normal BEAS-2B cells, suggesting potential therapeutic selectivity.
  • The observed modulation of apoptosis-related gene expression supports fisetin's mechanism of action and warrants further investigation for glioma treatment.
Keywords:
RT-PCRTEMcytotoxicityfisetinglioma

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