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- W2795665651 abstract "BACKGROUND:Like other human cancers, the malignancy of cervical cancer is also characterized by abilities of proliferation, migration, and invasion. Protein kinase C-zeta (PKCζ) has been highly correlated with several human cancers. Baicalin was proven to regulate PKC. This study aimed to investigate the anti-cancer effect and involved molecular mechanisms of baicalin on human cervical cancer. MATERIAL AND METHODS:Baicalin at various concentrations was used to treat 2 human cervical cancer cell lines HeLa and SiHa. The proliferation was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5 diphenylterazolium bromide (MTT) assay. The apoptosis was detected by terminal transferase UTP nick end labeling (TUNEL) assay. Wound healing assay and Transwell assay were used to evaluate the migration and invasion respectively. Western blotting was performed to assess the protein expression levels. RESULTS:Baicalin administration significantly reduced the viability by facilitating the apoptosis in HeLa and SiHa cells. Baicalin treatment also significantly reduced the wound closure and cell amount invaded as measured by Transwell assay. The expression levels of PKCζ, survivin, matrix metalloproteinase (MMP)2, MMP9 as well as the phosphorylation of signal transducer and activator of transcription (STAT) 3 were reduced in baicalin administrated cervical cancer cells. CONCLUSIONS:Baicalin exerted anti-cancer effects on human cervical cancer cells by targeting STAT3 regulated signaling pathways." @default.
- W2795665651 created "2018-04-13" @default.
- W2795665651 creator A5021129578 @default.
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- W2795665651 date "2018-04-03" @default.
- W2795665651 modified "2023-10-16" @default.
- W2795665651 title "Baicalin Inhibits Human Cervical Cancer Cells by Suppressing Protein Kinase C/Signal Transducer and Activator of Transcription (PKC/STAT3) Signaling Pathway" @default.
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- W2795665651 doi "https://doi.org/10.12659/msm.909640" @default.
- W2795665651 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5896362" @default.
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