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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Med+Sci+Monit
2018 ; 24
(ä): 1955-1961
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Baicalin Inhibits Human Cervical Cancer Cells by Suppressing Protein Kinase
C/Signal Transducer and Activator of Transcription (PKC/STAT3) Signaling Pathway
#MMPMID29610452
Wang Q
; Xu H
; Zhao X
Med Sci Monit
2018[Apr]; 24
(ä): 1955-1961
PMID29610452
show ga
BACKGROUND Like other human cancers, the malignancy of cervical cancer is also
characterized by abilities of proliferation, migration, and invasion. Protein
kinase C-zeta (PKC?) 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 PKC?, 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.
|Apoptosis/drug effects
[MESH]
|Cell Line, Tumor
[MESH]
|Cell Movement/drug effects
[MESH]
|Cell Proliferation/drug effects
[MESH]
|Female
[MESH]
|Flavonoids/*pharmacology
[MESH]
|HeLa Cells
[MESH]
|Humans
[MESH]
|Inhibitor of Apoptosis Proteins/metabolism
[MESH]