Mechanism of Biejiajian Wan Against EMT of Hepatocellular Carcinoma Cells Through NF-κB Signaling Pathway
10.13422/j.cnki.syfjx.20212421
- VernacularTitle:鳖甲煎丸通过NF-κB信号通路抑制肝癌细胞上皮间质转化的作用机制
- Author:
Xiao-dan ZHONG
1
;
Bin WEN
2
;
Hai-tao SUN
1
;
Jia-ling SUN
1
;
Xue-mei YANG
1
;
Wei-cong CHEN
1
;
Wen-ting ZHAO
3
;
Chun-yu HE
1
;
Yang LIU
1
;
Tong LI
1
;
Song-qi HE
1
Author Information
1. School of Chinese Medicine， Southern Medical University，Guangzhou 510515，China
2. Air Force Hospital of Southern Theater Command of PLA，Guangzhou 510602，China
3. Traditional Chinese Medicine-Integrated Hospital of Southern Medical University，Guangzhou 510315，China
- Publication Type:Journal Article
- Keywords:
hepatocellular carcinoma;
epithelial-mesenchymal transition;
Biejiajian Wan;
nuclear factor-kappa B （NF-κB） signaling pathway;
transforming growth factor-β1 （TGF-β1）
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2022;28(1):24-32
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the effect of Biejiajian Wan （BJJW） on transforming growth factor-β1 （TGF-β1）-induced epithelial-mesenchymal transition （EMT） of HepG2 cells， and explore its mechanism against EMT of hepatocellular carcinoma cells. MethodHepG2 cells were randomly divided into a blank group， a TGF-β1 model group （10 μg·L-1 TGF-β1）， a low-dose BJJW group （10 μg·L-1 TGF-β1+0.55 g·kg-1 BJJW）， a medium-dose BJJW group （10 μg·L-1 TGF-β1+1.1 g·kg-1 BJJW）， a high-dose BJJW group （10 μg·L-1 TGF-β1+2.2 g·kg-1 BJJW）， and a sorafenib group （10 μg·L-1 TGF-β1+0.03 g·kg-1 sorafenib）. The EMT model was induced by 10 μg·L-1 TGF-β1 in HepG2 cells. After treatment with corresponding medicated serum， cell counting kit -8 （CCK-8） assay was used to detect cell proliferation. Cell migration ability was detected by the Transwell assay and wound healing assay. The protein expression related to EMT and nuclear factor-kappa B （NF-κB） signaling pathway was detected by cell immunofluorescence assay and Western blot. ResultCompared with the blank group 4 days later， the TGF-β1 model group showed fusiform and loose cells with widened gap and antennae reaching out， decreased protein expression of E-cadherin （P<0.05）， and increased protein expression of N-cadherin and vimentin （P<0.05）， which indicated that the EMT model was properly induced in HepG2 cells by TGF-β1 stimulation for 4 days. After 48 hours of treatment with the corresponding medicated serum， each medication group showed inhibited proliferation of HepG2 cells that had undergone EMT， especially the low- and high-dose BJJW groups （P<0.01）， and the medium-dose BJJW group showed increased E-cadherin protein expression （P<0.05） and decreased p-p65， N-cadherin， and vimentin protein expression （P<0.05）， as compared with the TGF-β1 model group. As revealed by the transwell assay and wound healing assay， TGF-β1 enhanced the migration ability of HepG2 cells （P<0.05， P<0.01） compared with the results in the blank group， compared with the TGF-β1 model group， the medication groups showed inhibited migration ability of HepG2 cells （P<0.05， P<0.01）. Compared with the blank group， the TGF-β1 model group promoted the expression of p65 and Snail into the nucleus. Compared with the TGF-β1 model group， the medication groups inhibited the expression of p65 and Snail into the nucleus. ConclusionBJJW may inhibit the EMT， proliferation， and migration of HepG2 cells induced by TGF-β1 by suppressing the NF-κB signaling pathway to exert an anti-hepatocellular carcinoma effect.
