Induction of Apoptosis in Human Hepatocellular Carcinoma Cells by Erianin Involves a Mitochondria-Mediated Pathway

2020 ◽  
Vol 19 (3) ◽  
pp. 261-269
Author(s):  
Zhong Min ◽  
He Lei ◽  
Shi Yujie ◽  
Chen Xin ◽  
Ren Jianwu
Keyword(s):  
Hepatocellular Carcinoma ◽  
Antitumor Activity ◽  
Hepg2 Cells ◽  
Chinese Herb ◽  
Human Hepatocellular Carcinoma ◽  
Dependent Manner ◽  
M Cell ◽  
Cytochrome C Release ◽  
Intracellular Ca ◽  
Induced Apoptosis

Erianin is a natural product derived from the traditional Chinese herb, Dendrobium chrysotoxum, which is highly valued for its antitumor activity in various cancer cells. However, the specific mechanism of antitumor activity of erianin in human hepatocellular carcinoma remains unclear. This study aimed to investigate erianin-induced apoptosis in human hepatocellular carcinoma HepG2 cells. The proliferation of HepG2 cells was significantly inhibited by the treatment of erianin in a doseand time-dependent manner. In addition, erianin induced a series of apoptosis-related events in HepG2 cells, including G2/M cell cycle arrest, the loss of the mitochondrial membrane potential, elevation of intracellular Ca2+, and accumulation of reactive oxygen species. Erianin activated the caspase-3 and caspase-9 without a change in caspase-8, accompanied by upregulation of the expression of Bax and downregulation of the expression of Bcl-2 along with cytochrome C release from the mitochondria. There was no significant change in Fas and FasL expression, indicating that the exogenous pathway is not involved in erianin-induced apoptosis. In summary, it concluded that erianin-induced apoptosis in HepG2 cells is through a mitochondria-mediated pathway. The results of this study suggest that erianin may serve as a novel therapeutic agent for the treatment of human hepatocellular carcinoma in the future.

scholarly journals NeosedumosideIII induced Apoptosis of Human Hepatocellular Carcinoma HepG2 cells and SMMC-7721 Cells and Related Mechanism

2021 ◽  
Author(s):  
Xin-Yu Li ◽  
Xin Zhou ◽  
Yu- Liu ◽  
Feng Qiu ◽  
Qing-Qing Zhao
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Cycle ◽  
Hepg2 Cells ◽  
Caspase 3 ◽  
Human Hepatocellular Carcinoma ◽  
Caspase 8 ◽  
Dependent Manner ◽  
Caspase 9 ◽  
Induced Apoptosis

Abstract Purpose: NeosedumosideIII (Neo) is a megastigmanes and belongs to monocyclic sesquiterpenoids compound with antioxidant, anti-inflammatory and other pharmacological activities. In order to explore the anti-cancer effect and possible mechanism of Neo, the study examined the anti-proliferation and apoptosis effect of Neo against human hepatocellular carcinoma HepG2 cells and SMMC-772 cells and related mechanism in vitro. Methods ：The anti-proliferation effect of Neo was detected on HepG2 cells and SMMC-772 cells by MTT assay and IC50 with increasing dose and time. Cell cycle and apoptosis were detected by flow cytometer. The changes of Bcl-2, Bax, Caspase-3, Caspase-8 and Caspase-9 proteins were detected by western blotting.Results ：The results indicated that Neo could inhibited proliferation of HepG2 cells and SMMC-772 cells in vitro and promoted apoptosis, it significantly induced apoptosis of HepG2 cells and SMMC-772 cells arrested cell cycle at G0/G1 phase in a dose-dependent manner, reduce the expression of Bcl-2 protein, and increase the expression of Bax and Caspase-3, Caspase-8 and Caspase-9 proteins. Conclusion：Neo could inhibit proliferation and induce apoptosis of HepG2 cells and SMMC-7721 cells in vivo which suggested that it might be served as a promising candidate for the treatment of liver cancer.

scholarly journals Effects of Lidocaine-Mediated CPEB3 Upregulation in Human Hepatocellular Carcinoma Cell Proliferation In Vitro

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Hongjun Liu ◽  
Yiru Wang ◽  
Bing Chen ◽  
Xia Shen ◽  
Wenxian Li
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Antitumor Activity ◽  
Cell Viability ◽  
Hepg2 Cell ◽  
Hepg2 Cells ◽  
Human Hepatocellular Carcinoma ◽  
Dependent Manner ◽  
Real Time Quantitative Pcr

Lidocaine displays antitumor activity by inducing apoptosis and suppressing tumor growth in human hepatocellular carcinoma (HepG2) cells in vitro. However, the molecular mechanism underlying lidocaine-mediated antitumor activity is unclear. In this study, HepG2 cells were treated with lidocaine, and cell proliferation and colony-forming ability were assessed. The expression level of cytoplasmic polyadenylation element binding protein 3 (CPEB3) was detected by real-time quantitative PCR and western blot. Lidocaine treatment resulted in decreased HepG2 cell viability and colony formation in a dose-dependent manner. In hepatocellular carcinoma patient samples, CPEB3 was downregulated and was associated with poor prognosis and high-grade malignancy. Additionally, CPEB3 was a critical mediator of lidocaine-induced repression of HepG2 cell proliferation. These results demonstrated that lidocaine decreased cell viability and colony-forming ability of HepG2 cells by upregulating CPEB3 expression.

The Effect and Mechanism of Apoptosis Induced by Desacetylcinobufotalin (DEBF) in Human Hepatocellular Carcinoma HepG2 Cells

2013 ◽  
Vol 395-396 ◽  
pp. 587-590
Author(s):  
Xu Chao ◽  
Lin Dang ◽  
Min Hui Wei
Keyword(s):  
Hepatocellular Carcinoma ◽  
Antitumor Activity ◽  
Western Blot ◽  
Hepg2 Cells ◽  
Human Hepatocellular Carcinoma ◽  
Inhibition Effect ◽  
Marked Inhibition ◽  
Mitochondria Pathway

The cytotoxicity of Desacetylcinobufotalin (DEBF) and apoptosis induced by DEBF was measured. Additionally the mechanism of Apoptosis induced by DEBF was studied through Western blot. The results show DEBF displayed the marked inhibition effect to HepG2 cells and the IC50value is 0.0279μmol/ml. The expression of Bax was significantly increased and the expression of Bcl-2 was markedly decreased, compared to the control. The data suggest DEBF had significant antitumor activity through induction apoptosis via mitochondria pathway.

NCPMF-60 induces G2/M cell cycle arrest and apoptosis in human hepatocellular carcinoma HepG2 cells

2011 ◽  
Vol 22 (1) ◽  
pp. 46-57 ◽  
Author(s):  
Qin-Sheng Dai ◽  
Wei Liu ◽  
Xiao-Bing Wang ◽  
Na Lu ◽  
Dan-Dan Gong ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Hepg2 Cells ◽  
Human Hepatocellular Carcinoma ◽  
M Cell ◽  
Cycle Arrest

scholarly journals The effects and mechanism of peiminine-induced apoptosis in human hepatocellular carcinoma HepG2 cells

PLoS ONE ◽  
2019 ◽  
Vol 14 (1) ◽  
pp. e0201864 ◽  
Author(s):  
Xu Chao ◽  
Guoquan Wang ◽  
Yuping Tang ◽  
Changhu Dong ◽  
Hong Li ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Hepg2 Cells ◽  
Human Hepatocellular Carcinoma ◽  
Induced Apoptosis

Sensitization of TRAIL-induced apoptosis in human hepatocellular carcinoma HepG2 cells by phytochemicals

Life Sciences ◽  
2013 ◽  
Vol 92 (10) ◽  
pp. 555-561 ◽  
Author(s):  
Reem N. Abou El Naga ◽  
Samar S. Azab ◽  
Ebtehal El-Demerdash ◽  
Sabry Shaarawy ◽  
Mahmoud El-Merzabani ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Hepg2 Cells ◽  
Human Hepatocellular Carcinoma ◽  
Induced Apoptosis

Lidocaine Induces Apoptosis and Suppresses Tumor Growth in Human Hepatocellular Carcinoma Cells In Vitro and in a Xenograft Model In Vivo

2017 ◽  
Vol 126 (5) ◽  
pp. 868-881 ◽  
Author(s):  
Wei Xing ◽  
Dong-Tai Chen ◽  
Jia-Hao Pan ◽  
Yong-Hua Chen ◽  
Yan Yan ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Cycle ◽  
Antitumor Activity ◽  
Hepg2 Cells ◽  
Xenograft Model ◽  
Mitogen Activated Protein Kinase ◽  
Dependent Manner ◽  
Bax Protein

Abstract Background Recent epidemiologic studies have focused on the potential beneficial effects of regional anesthetics, and the differences in cancer prognosis may be the result of anesthetics on cancer biologic behavior. However, the function and underlying mechanisms of lidocaine in hepatocellular carcinoma both in vitro and in vivo have been poorly studied. Methods Human HepG2 cells were treated with lidocaine. Cell viability, colony formation, cell cycle, and apoptosis were assessed. The effects of lidocaine on apoptosis-related and mitogen-activated protein kinase protein expression were evaluated by Western blot analysis. The antitumor activity of lidocaine in hepatocellular carcinoma with or without cisplatin was investigated with in vitro experiments and also with animal experiments. Results Lidocaine inhibited the growth of HepG2 cells in a dose- and time-dependent manner. The authors also found that lidocaine arrested cells in the G0/G1 phase of the cell cycle (63.7 ± 1.7% vs. 72.4 ± 3.2%; P = 0.0143) and induced apoptosis (1.7 ± 0.3% vs. 5.0 ± 0.7%; P = 0.0009). Lidocaine may exert these functions by causing an increase in Bax protein and activated caspase-3 and a corresponding decrease in Bcl-2 protein through the extracellular signal-regulated kinase 1/2 and p38 pathways. More importantly, for the first time, xenograft experiments (n = 8 per group) indicated that lidocaine suppressed tumor development (P < 0.0001; lidocaine vs. control) and enhanced the sensitivity of cisplatin (P = 0.0008; lidocaine plus cisplatin vs. cisplatin). Conclusions The authors’ findings suggest that lidocaine may exert potent antitumor activity in hepatocellular carcinoma. Furthermore, combining lidocaine with cisplatin may be a novel treatment option for hepatocellular carcinoma.

Involvement of NF-κB activation in the apoptosis induced by extracellular adenosine in human hepatocellular carcinoma HepG2 cellsThis paper is one of a selection of papers published in this special issue entitled “Second International Symposium on Recent Advances in Basic, Clinical, and Social Medicine” and has undergone the Journal's usual peer review process.

2010 ◽  
Vol 88 (4) ◽  
pp. 705-714 ◽  
Author(s):  
Ling-Fei Wu ◽  
Guo-Ping Li ◽  
Jian-Dong Su ◽  
Ze-Jin Pu ◽  
Jia-Lin Feng ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Cycle ◽  
Flow Cytometry ◽  
Mtt Assay ◽  
Cell Apoptosis ◽  
Hepg2 Cells ◽  
Caspase 3 ◽  
Human Hepatocellular Carcinoma ◽  
Pyrrolidine Dithiocarbamate ◽  
Dependent Manner

Adenosine can exhibit cytotoxic activity in vivo and in vitro, though its mechanisms are still uncertain. In this study, we investigated the adenosine-mediated apoptotic signaling pathway and the role of NF-κB in human hepatocellular carcinoma HepG2 cells. HepG2 cells were treated with different concentrations of adenosine for 12–48 h, and the effect of adenosine on cell proliferation was evaluated by MTT assay. The cytotoxicity of adenosine alone or in combination with an NF-κB inhibitor, pyrrolidine dithiocarbamate (PDTC), was also evaluated by MTT assay and the mode of cell death was detected by Hoechst 33342 staining. Cell cycle progress was performed by flow cytometry with PI staining. The protein expressions of Bcl-2, p53, NF-κB subunit p65, and caspase-3 were assayed by Western blot. Caspase-3 activity was measured by spectrophotomteric assay. The results showed that adenosine significantly reduced the viability of HepG2 cells in a dose- and time-dependent manner, with IC 50 (24 and 48 h) of 2.52 and 1.89 mmol·L–1, respectively. The apoptotic index (percentage of sub-G1 phase) of HepG2 cells in adenosine treatment alone for 12 and 24 h or in combination with PDTC were 8.30%, 22.32% and 20.18%, 30.89%, respectively. All of them were higher than that in the control group (0.81%, p < 0.01). The characteristic changes of cell apoptosis (chromatin condensation and sub-G1 peak) were observed under fluorescent microscopy and flow cytometry. We also found that the apoptotic process triggered by adenosine was involved in G0–G1 cell-cycle arrest, enhanced the activity of caspase-3, upregulated p53 and NF-κB p65 expression, and downregulated Bcl-2 expression. Inhibition of NF-κB by PDTC decreased NF-κB p65 expression, enhanced cell apoptosis ratio, and increased caspase-3 activity. NF-κB may play an anti-apoptosis role in adenosine-induced HepG2 cytotoxicity.

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