scholarly journals Effects of harmaline on cell growth of human liver cancer through the p53/p21 and Fas/FasL signaling pathways

2017 ◽  
Author(s):  
Bin Xu ◽  
Minpeng Li ◽  
Yuan Yu ◽  
Jun He ◽  
Siqin Hu ◽  
...  
Keyword(s):  
Cell Growth ◽  
Liver Cancer ◽  
Signaling Pathways ◽  
Human Liver ◽  
Human Liver Cancer

scholarly journals Cordycepin induces apoptosis in human liver cancer HepG2 cells through extrinsic and intrinsic signaling pathways

2016 ◽  
Vol 12 (2) ◽  
pp. 995-1000 ◽  
Author(s):  
Le-Wen Shao ◽  
Li-Hua Huang ◽  
Sheng Yan ◽  
Jian-Di Jin ◽  
Shao-Yan Ren
Keyword(s):  
Liver Cancer ◽  
Signaling Pathways ◽  
Hepg2 Cells ◽  
Human Liver ◽  
Human Liver Cancer

Activation of PPARΓ inhibits cell growth and induces apoptosis in human liver cancer cells

2000 ◽  
Vol 118 (4) ◽  
pp. A921
Author(s):  
Mitsuo Toyoda ◽  
Hitoshi Takagi ◽  
Norio Horiguchi ◽  
Hisashi Takayama ◽  
Ken Sato ◽  
...  
Keyword(s):  
Cell Growth ◽  
Liver Cancer ◽  
Cancer Cells ◽  
Human Liver ◽  
Liver Cancer Cells ◽  
Human Liver Cancer ◽  
Human Liver Cancer Cells

scholarly journals Sedanolide induces autophagy through the PI3K, p53 and NF-κB signaling pathways in human liver cancer cells

2015 ◽  
Vol 47 (6) ◽  
pp. 2240-2246 ◽  
Author(s):  
SHU-LING HSIEH ◽  
CHI-TSAI CHEN ◽  
JYH-JYE WANG ◽  
YU-HAO KUO ◽  
CHIEN-CHUN LI ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Signaling Pathways ◽  
Human Liver ◽  
Liver Cancer Cells ◽  
Human Liver Cancer ◽  
Human Liver Cancer Cells

scholarly journals Engelharquinone suppresses lipopolysaccharide-induced inflammation and proliferation of human liver cancer SMCC7721 cells via inhibition of NF-κB and MAPK signaling pathway

2020 ◽  
Vol 19 (4) ◽  
pp. 699-706
Author(s):  
Shan Li ◽  
Yan Zhang ◽  
Aishe Gao ◽  
Yue Zhang ◽  
Jiong Zhang
Keyword(s):  
Liver Cancer ◽  
Tumor Growth ◽  
Signaling Pathways ◽  
Inflammatory Cytokines ◽  
Human Liver ◽  
Mapk Signaling ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Human Liver Cancer ◽  
Mapk Signaling Pathways

Purpose: To investigate the anti-tumor effect of engelharquinone (Eng) on human liver cancer SMCC7721 cells.Methods: GFP-labeled SMCC7721 cells were used to establish a tumor-bearing mice model used for determination of the effect of different  concentrations of Eng on tumor growth. The effect of Eng on SMCC7721 cell viability was determined with MTT assay and cell cycle analysis. The anti-inflammatory effect of Eng on lipopolysaccharide (LPS)-treated SMCC7721 cells were determined through assay of pro-inflammatory cytokines. Besides, the effect of Eng on the expressions of mitogen-activated protein kinase (MAPK), toll-like receptor 4 (TLR4), and nuclear factor kappa B (NF-κB) was determined.Results: Cell proliferation was suppressed by different concentrations of Eng in LPS-treated SMCC7721 cells. Treatment of nude mice with Eng at high and low doses resulted in significant suppression of tumor growth and marked increases in percentage survival. Treatment of SMCC7721 cells with LPS upregulated the expressions of NF-κB, p65 and MAPK. However, pre-treatment of the cells with Eng suppressed the LPS-induced upregulation of the NF-κB, p65 and MAPK signaling pathways, and further downregulated the production of inflammatory cytokines in SMCC7721 cells.Conclusion: These results indicate that Eng inhibits LPS-induced inflammation and proliferation of human liver cancer SMCC7721 cells via a mechanism involving regulation of NF-κB and MAPK signaling pathways. Thus, Eng has potentials for the clinical management of inflammatory diseases and liver cancer. Keywords: Inflammation, Engelharquinone, Lipopolysaccharide, SMCC7721 cells, Toll-like receptor 4

Precise Electrical Detection of Curcumin Cytotoxicity in Human Liver Cancer Cells

2021 ◽  
Author(s):  
Novi Angeline ◽  
Sung-Sik Choo ◽  
Cheol-Hwi Kim ◽  
Suk Ho Bhang ◽  
Tae-Hyung Kim
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Human Liver ◽  
Electrical Detection ◽  
Liver Cancer Cells ◽  
Human Liver Cancer ◽  
Human Liver Cancer Cells

scholarly journals Inhibition of human liver cancer cell growth by evodiamine involves apoptosis and deactivation of PI3K/AKT pathway

2020 ◽  
Vol 63 (1) ◽  
Author(s):  
Jia Jia ◽  
Xigang Kang ◽  
Yanfang Liu ◽  
Jianwei Zhang
Keyword(s):  
Liver Cancer ◽  
Cancer Cell ◽  
Human Liver ◽  
Akt Pathway ◽  
Migration And Invasion ◽  
Dependent Manner ◽  
Liver Cancer Cell ◽  
Human Liver Cancer Cell ◽  
Human Liver Cancer ◽  
Induction Of Apoptosis

Abstract Evodiamine is an active alkaloid member found in Traditional Chinese Herb (TCH) Evodia rutaecarpa. It has been reported to exhibit remarkable biological and medicinal activities including anticancer and anti-inflammatory. This study was designed to investigate the anticancer effects of evodiamine against human liver cancer and evaluate its effects on cell migration, cell invasion, cellular apoptosis and PI3K/AKT pathway. The results showed that evodiamine exhibits potent antiproliferative effects against two human liver cancer cell lines (HepG2 and PLHC-1) with an IC50 of 20 µM. Nonetheless, the cytotoxic effects of evodiamine were comparatively low against the normal cells as evident from the IC50 of 100 μM. The growth inhibitory effects of evodiamine were found to be due to the induction of apoptosis as revealed by the DAPI, AO/EB and annexin V/PI staining assays. The induction of apoptosis was also associated with upregulation of Bax and downregulation of Bcl-2 expression in a concentration dependent manner. The wound healing and transwell assay revealed that evodiamine caused a significant decline in the migration and invasion of the HepG2 and PLHC-1 cells. Investigation of the effects of evodiamine on the PI3K/AKT signalling revealed that evodiamine inhibited the phosphorylation of PI3K and AKT proteins. Taken together, the results showed that evodiamine inhibits the growth of human liver cancer via induction of apoptosis and deactivation of PI3K/AKT pathway. The results point towards the therapeutic potential of evodiamine in the treatment of liver cancer.

Sign in / Sign up

Export Citation Format

Share Document