Lectin from Dioclea violacea induces autophagy in U87 glioma cells

Ana Paula M Nascimento1, Ingrid A V Wolin1, Priscilla G Welter1

  • 1Departamento de Bioquímica e Programa de Pós-graduação em Bioquímica, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, Campus Universitário, 88040-900 Florianópolis, Santa Catarina, Brazil.

Insights

Dioclea violacea lectin (DVL) shows selective antitumor activity against U87 human glioma cells by inhibiting proliferation and migration. DVL induces cell death partially through autophagy, offering a potential new therapeutic strategy.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Pharmacology

Background:

  • Lectins are carbohydrate-binding proteins with diverse biological activities.
  • Glioma is a primary brain tumor with limited treatment options.
  • Dioclea violacea lectin (DVL) is a plant lectin with potential therapeutic applications.

Purpose of the Study:

  • To evaluate the antitumor activity of DVL on human glioma cells.
  • To compare DVL's efficacy with Canavalia ensiformis lectin (ConA).
  • To elucidate the mechanisms underlying DVL's cytotoxic effects.

Main Methods:

  • U87 human glioma cell line and primary astrocyte cultures were used.
  • Cell viability, proliferation, migration, and clonogenic survival were assessed.
  • Mechanisms including mitochondrial potential, ROS, caspase activation, autophagy, and signaling pathways (Akt, mTORC1, ERK, JNK, p38 MAPK) were analyzed.

Main Results:

  • DVL significantly reduced glioma cell viability, proliferation, and migration in a dose- and time-dependent manner.
  • DVL induced cell death via disruption of mitochondrial potential and autophagy, independent of apoptosis.
  • DVL modulated signaling pathways, decreasing Akt/mTORC1/ERK phosphorylation and increasing JNK/p38 MAPK phosphorylation.
  • DVL demonstrated higher potency than ConA and selectively spared normal astrocytes.

Conclusions:

  • DVL exhibits selective antitumor activity against human glioma cells.
  • DVL's mechanism involves inhibiting cell migration and proliferation, inducing autophagy, and altering key signaling pathways.
  • DVL represents a promising candidate for glioma therapy, warranting further investigation.

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