Effects of Amphidinium carterae Phytocompounds on Proliferation and the Epithelial–Mesenchymal Transition Process in T98G Glioblastoma Cells

TL;DR

This study explores how compounds from the microalgae Amphidinium carterae affect the growth and EMT process in glioblastoma cells, suggesting potential new treatments for brain cancer.

Contribution

The study introduces the potential of A. carterae-derived compounds to target EMT in glioblastoma, a novel approach for cancer therapy.

Findings

Different A. carterae strains modulate EMT markers in T98G glioblastoma cells.

The compounds affect the proliferation and migration of GBM cells.

This research highlights marine microalgae as a source of anticancer agents.

Abstract

Glioblastoma (GBM) is an aggressive type of brain cancer, frequently invasive, with a low survival rate and complicated treatment. Recent studies have shown the modulation of epithelial–mesenchymal transition (EMT) biomarkers in glioblastoma cells associated with tumor progression, chemoresistance, and relapse after treatment. GBM handlings are based on aggressive chemical therapies and surgical resection with poor percentage of survival, boosting the search for more specific remedies. Marine eukaryotic microalgae are rapidly advancing as a source of anticancer drugs due to their ability to produce potent secondary metabolites with biological activity. Among such microalgae, dinoflagellates, belonging to the species Amphidinium carterae, are known producers of neurotoxins and cytotoxic compounds. We tested the capability of chemical extracts from two different strains of A. carterae to modulate the EMT markers in T98G, human GBM cells. In vitro proliferation and migration studies and EMT biomarkers’ abundance and modulation assays showed that the different A. carterae strains differently modulated both EMT markers and the proliferation/migration capability of GBM cells. This study sets the bases to find a marine microalgae-derived natural compound that could potentially target the epithelial–mesenchymal transition in brain-derived tumor types.

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