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Published on: July 20, 2019
Nicotinic acid inhibits glioma invasion by facilitating Snail1 degradation
Jiejing Li1,2, Jiagui Qu1, Yu Shi3,4
1Department of Clinical Laboratory, The Affiliated Hospital of KMUST, Medical School, Kunming University of Science and Technology, Kunming 650032, China.
Abstract:
Malignant glioma is a formidable disease that commonly leads to death, mainly due to the invasion of tumor cells into neighboring tissues. Therefore, inhibition of tumor cell invasion may provide an effective therapy for malignant glioma. Here we report that nicotinic acid (NA), an essential vitamin, inhibits glioma cell invasion in vitro and in vivo. Treatment of the U251 glioma cells with NA in vitro results in reduced invasion, which is accompanied by a loss of mesenchymal phenotype and an increase in cell-cell adhesion. At the molecular level, transcription of the adherens junction protein E-cadherin is upregulated, leading to accumulation of E-cadherin protein at the cell-cell boundary. This can be attributed to NA's ability to facilitate the ubiquitination and degradation of Snail1, a transcription factor that represses E-cadherin expression. Similarly, NA transiently inhibits neural crest migration in Xenopus embryos in a Snail1-dependent manner, indicating that the mechanism of action for NA in cell migration is evolutionarily conserved. We further show that NA injection blocks the infiltration of tumor cells into the adjacent brain tissues and improves animal survival in a rat model of glioma. These results suggest that NA treatment may be developed into a potential therapy for malignant glioma.
Insights
Nicotinic acid (NA) effectively inhibits malignant glioma cell invasion by upregulating E-cadherin and downregulating Snail1. This vitamin therapy shows promise for treating glioma by blocking tumor cell infiltration and improving survival rates.
Area of Science:
- Oncology
- Molecular Biology
- Neuroscience
Background:
- Malignant glioma is a fatal brain tumor characterized by aggressive cell invasion.
- Inhibiting tumor cell invasion is a critical therapeutic strategy for malignant glioma.
- Nicotinic acid (NA), an essential vitamin, has potential anti-cancer properties.
Purpose of the Study:
- To investigate the effect of nicotinic acid (NA) on glioma cell invasion.
- To elucidate the molecular mechanisms underlying NA's action on glioma cells.
- To evaluate the therapeutic potential of NA in preclinical glioma models.
Main Methods:
- In vitro studies using U251 glioma cells treated with NA.
- Analysis of cell invasion, mesenchymal phenotype, and cell-cell adhesion.
- Molecular analysis of E-cadherin and Snail1 expression and localization.
- In vivo studies using Xenopus embryos and a rat glioma model.
Main Results:
- NA treatment reduced glioma cell invasion in vitro and in vivo.
- NA induced a loss of mesenchymal phenotype and increased cell-cell adhesion.
- NA upregulated E-cadherin transcription and protein levels by promoting Snail1 ubiquitination and degradation.
- NA inhibited neural crest cell migration in Xenopus embryos in a Snail1-dependent manner.
- NA injection reduced tumor cell infiltration and improved survival in a rat glioma model.
Conclusions:
- Nicotinic acid inhibits glioma cell invasion through a conserved Snail1-dependent mechanism.
- NA's ability to upregulate E-cadherin offers a potential therapeutic strategy for malignant glioma.
- Nicotinic acid represents a promising candidate for novel glioma therapies.
