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Wogonin Inhibits Nasopharyngeal Carcinoma Cells

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Wogonin, an active constituent of Scutellaria baicalensis Georgi, exhibits antitumor potential. This study aimed to study the effect and mechanism of wogonin on the apoptosis and proliferation of nasopharyngeal carcinoma cells. Methyl thiazolyl tetrazolium-based cell viability, flow cytometry, and Transwell assays were conducted to assess the cells’ malignant behaviors, and western blot was utilized to assess protein expression. The results indicated that wogonin inhibited nasopharyngeal carcinoma cell proliferation, migration, invasion, and elevated cell apoptosis in a dose-dependent way. Besides, wogonin inhibited miR-150 expression in nasopharyngeal carcinoma cells in a dose-dependent way. After transfection with a miR-150 inhibitor, the proliferation, migration, and invasion of nasopharyngeal carcinoma cells were hindered, while the apoptosis rate was enhanced. Moreover, miR-150 reduction increased phosphatase and tensin homolog expression while decreasing p-Akt expression in cells. Rescue assays further validated that phosphatase and tensin homolog silencers reversed the impacts of miR-150 downregulation on nasopharyngeal carcinoma cells malignant behaviors, and miR-150 elevation reversed the impacts of wogonin on nasopharyngeal carcinoma cells’ malignant behaviors. To sum up, wogonin inhibited nasopharyngeal carcinoma cell proliferation, migration, and invasion via the miR-150/phosphatase and tensin homolog/Akt axes.
Title: Wogonin Inhibits Nasopharyngeal Carcinoma Cells
Description:
Wogonin, an active constituent of Scutellaria baicalensis Georgi, exhibits antitumor potential.
This study aimed to study the effect and mechanism of wogonin on the apoptosis and proliferation of nasopharyngeal carcinoma cells.
Methyl thiazolyl tetrazolium-based cell viability, flow cytometry, and Transwell assays were conducted to assess the cells’ malignant behaviors, and western blot was utilized to assess protein expression.
The results indicated that wogonin inhibited nasopharyngeal carcinoma cell proliferation, migration, invasion, and elevated cell apoptosis in a dose-dependent way.
Besides, wogonin inhibited miR-150 expression in nasopharyngeal carcinoma cells in a dose-dependent way.
After transfection with a miR-150 inhibitor, the proliferation, migration, and invasion of nasopharyngeal carcinoma cells were hindered, while the apoptosis rate was enhanced.
Moreover, miR-150 reduction increased phosphatase and tensin homolog expression while decreasing p-Akt expression in cells.
Rescue assays further validated that phosphatase and tensin homolog silencers reversed the impacts of miR-150 downregulation on nasopharyngeal carcinoma cells malignant behaviors, and miR-150 elevation reversed the impacts of wogonin on nasopharyngeal carcinoma cells’ malignant behaviors.
To sum up, wogonin inhibited nasopharyngeal carcinoma cell proliferation, migration, and invasion via the miR-150/phosphatase and tensin homolog/Akt axes.

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