Epigenetic Modification and Differentiation Induction of Malignant Glioma Cells by Oligo-Fucoidan
Liao CH., Lai IC., Kuo HC., Chuang SE., Lee HL., Whang-Peng J.
Clinical Trial, published in Mar Drugs (2019) — summary generated from the PubMed abstract.
Several human studies show positive signals, while research methods and sample sizes continue to develop.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Clinical Trial
- Journal
- Mar Drugs (2019)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 31500384
- PMCID
- PMC6780514
- DOI
- 10.3390/md17090525
- Citations
- 17
Abstract (original English)
Malignant glioma (MG) is a poor prognostic brain tumor with inevitable recurrence after multimodality treatment. Searching for more effective treatment is urgently needed. Differentiation induction via epigenetic modification has been proposed as a potential anticancer strategy. Natural products are known as fruitful sources of epigenetic modifiers with wide safety margins. We thus explored the effects of oligo-fucoidan (OF) from brown seaweed on this notion in MG cells including Grade III U87MG cells and Grade IV glioblastoma multiforme (GBM)8401 cells and compared to the immortalized astrocyte SVGp12 cells. The results showed that OF markedly suppress the proliferation of MG cells and only slightly affected that of SVGp12 cells. OF inhibited the protein expressions of DNA methyltransferases 1, 3A and 3B (DNMT1, 3A and 3B) accompanied with obvious mRNA induction of differentiation markers ( MBP , OLIG2 , S100β , GFAP , NeuN and MAP2 ) both in U87MG and GBM8401 cells. Accordingly, the methylation of p21 , a DNMT3B target gene, was decreased by OF. In combination with the clinical DNMT inhibitor decitabine, OF could synergize the growth inhibition and MBP induction in U87MG cells. Appropriated clinical trials are warranted to evaluate this potential complementary approach for MG therapy after confirmation of the effects in vivo.
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
Evidence level
Several human studies show positive signals, while research methods and sample sizes continue to develop.
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