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

Antitumor Activity ◽

Western Blot ◽

Hepg2 Cells ◽

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.

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

Current Topics in Nutraceutical Research ◽

10.37290/ctnr2641-452x.19:261-269 ◽

2020 ◽

Vol 19 (3) ◽

pp. 261-269

Author(s):

Zhong Min ◽

He Lei ◽

Shi Yujie ◽

Chen Xin ◽

Ren Jianwu

Keyword(s):

Antitumor Activity ◽

Hepg2 Cells ◽

Chinese Herb ◽

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.

Reactive oxygen species-mitochondria pathway involved in LYG-202-induced apoptosis in human hepatocellular carcinoma HepG2 cells

Cancer Letters ◽

10.1016/j.canlet.2010.04.004 ◽

2010 ◽

Vol 296 (1) ◽

pp. 96-105 ◽

Cited By ~ 23

Author(s):

Fei-hong Chen ◽

Lin-bo Zhang ◽

Lei Qiang ◽

Zhen Yang ◽

Tian Wu ◽

...

Keyword(s):

Reactive Oxygen Species ◽

Hepg2 Cells ◽

Reactive Oxygen ◽

Oxygen Species ◽

Mitochondria Pathway ◽

Induced Apoptosis

Reactive oxygen species–mitochondria pathway involved in FV-429-induced apoptosis in human hepatocellular carcinoma HepG2 cells

Anti-Cancer Drugs ◽

10.1097/cad.0b013e3283483d65 ◽

2011 ◽

Vol 22 (9) ◽

pp. 886-895 ◽

Cited By ~ 5

Author(s):

Zhen Yang ◽

Lei Qiang ◽

Tian Wu ◽

Fei-Hong Chen ◽

Hui-Ying Yang ◽

...

Keyword(s):

Reactive Oxygen Species ◽

Hepg2 Cells ◽

Reactive Oxygen ◽

Oxygen Species ◽

Mitochondria Pathway ◽

Induced Apoptosis

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

BioMed Research International ◽

10.1155/2018/8403157 ◽

2018 ◽

Vol 2018 ◽

pp. 1-7 ◽

Cited By ~ 2

Author(s):

Hongjun Liu ◽

Yiru Wang ◽

Bing Chen ◽

Xia Shen ◽

Wenxian Li

Keyword(s):

Cell Proliferation ◽

Antitumor Activity ◽

Cell Viability ◽

Hepg2 Cell ◽

Hepg2 Cells ◽

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 Antitumor Effects of Britanin on Hepatocellular Carcinoma Cells and its Real-Time Evaluation by In Vivo Bioluminescence Imaging

Anti-Cancer Agents in Medicinal Chemistry ◽

10.2174/1871520620666200227092623 ◽

2020 ◽

Vol 20 (9) ◽

pp. 1147-1156

Author(s):

Hanrui Li ◽

GeTao Du ◽

Lu Yang ◽

Liaojun Pang ◽

Yonghua Zhan

Keyword(s):

Western Blot ◽

Blot Analysis ◽

Tumor Size ◽

Hepg2 Cells ◽

Western Blot Analysis ◽

Bioluminescence Imaging ◽

Antitumor Effects ◽

In Vivo Bioluminescence Imaging

Background: Hepatocellular carcinoma is cancer with many new cases and the highest mortality rate. Chemotherapy is the most commonly used method for the clinical treatment of hepatocellular carcinoma. Natural products have become clinically important chemotherapeutic drugs due to their great potential for pharmacological development. Many sesquiterpene lactone compounds have been proven to have antitumor effects on hepatocellular carcinoma. Objective: Britanin is a sesquiterpene lactone compound that can be considered for the treatment of hepatocellular carcinoma. The present study aimed to investigate the antitumor effect of britanin. Methods: BEL 7402 and HepG2 cells were used to study the cytotoxicity and antitumor effects of britanin. Preliminary studies on the nuclear factor kappa B pathway were conducted by western blot analysis. A BEL 7402-luc subcutaneous tumor model was established for the in vivo antitumor studies of britanin. In vivo bioluminescence imaging was conducted to monitor changes in tumor size. Results: The results of the cytotoxicity analysis showed that the IC50 values for britanin in BEL 7402 and HepG2 cells were 2.702μM and 6.006μM, respectively. The results of the colony formation demonstrated that the number of cells in a colony was reduced significantly after britanin treatment. And the results of transwell migration assays showed that the migration ability of tumor cells was significantly weakened after treatment with britanin. Tumor size measurements and staining results showed that tumor size was inhibited after britanin treatment. The western blot analysis results showed the inhibition of p65 protein expression and reduced the ratio of Bcl-2/Bax after treatment. Conclusion: A series of in vitro and in vivo experiments demonstrated that britanin had good antitumor effects and provided an option for hepatocellular carcinoma treatment.