English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Tools annual

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Presents the access of premium content as premium feature

Premium Content

Global: Zendy Plus annual

Global: Zendy Free Plan

Background   Glioma is the most common malignant brain tumor and the patients are prone to poor prognosis. Due to limited treatments, new drug exploration has become a general trend. Therefore, the objective of this study is to investigate the effect of the new drugs C 18 H 17 NO 6  and its combination with Scutellarin on glioma cells and the underlying mechanism.Method   U251 and LN229 cells were administrated with C 18 H 17 NO 6  and its combination with Scutellarin. The proliferation ability of glioma cells was determined by cell counting kit-8, plate clone formation assay, and EdU incorporation assay. The cell cycle and apoptosis detection were detected by flow cytometry. Moreover, TUNEL assay was also used for cell apoptosis analysis. Then, the transfer ability of cells was achieved through wound healing assay. Furthermore, polymerase chain reaction (PCR) test and western bolt analysis were used to detect the mRNA expression and protein expression, respectively. Lastly, immunofluorescence was for the purity identification of astrocyte.Result   The results showed that, with the increasing dose of C 18 H 17 NO 6 , the cell inhibition rate, the cells in G1 phase, and the apoptosis rate were gradually increased, but the clone number, proliferation rate, and the cells in G2 and S phases were gradually decreased in comparison with control group. However, with the increase of C 18 H 17 NO 6 , the transferred rate of U251 and LN229 was not significantly augmented, expect that on U251 in C 18 H 17 NO 6  5  μ M group. In addition, Scutellarin 200  μ M has little effect on proliferation, with the inhibition rate 10-20% and proliferation rate except U251 in Scutellarin 200  μ M group similar to that in control group. Moreover, compared to control group, Scutellarin 300  μ M increased the U251 cells in G2 and S phases and the apoptosis rate of LN229 but decreased the LN229 cells in G2 and S phases. Besides, in Scutellarin 200  μ M group, the transfer ability of LN229 was inhibited, but not in U251. Furthermore, if C 18 H 17 NO 6  was combined with Scutellarin 200/300 μ M, the proliferation and transferred ability were suppressed and the apoptosis was elevated in LN229 cell in comparison with C 18 H 17 NO 6  alone. Dramatically, the combined effect on U251 was the exact opposite. Importantly, there was little toxicity on astrocyte under the dose of C 18 H 17 NO 6  and Scutellarin in the study. In molecular level, the mRNA and protein expression of Fas-associated factor 1 (FAF1) expression in U251 and LN229 were upregulated by C 18 H 17 NO 6  and its combination with Scutellarin, especially the protein expression.Conclusion   C 18 H 17 NO 6  could efficiently suppress cell proliferation and induce cell apoptosis in glioma cells, and its combination with Scutellarin had a promoting effect, in which the underlying mechanism referred to the upregulation of Fas-associated factor 1.

biomed research international

C18H17NO6and Its Combination with Scutellarin Suppress the Proliferation and Induce the Apoptosis of Human Glioma Cells via Upregulation of Fas-Associated Factor 1 Expression