NF-KB inhibitor suppresses TNF-a and chemothera-peutic agents-induced apoptosis in hepG2 cells

2000 ◽  
Vol 118 (4) ◽  
pp. A1500
Author(s):  
Takenari Yamanaka ◽  
Katsuya Shiraki ◽  
Hidekazu Inoue ◽  
Takeshi Ito ◽  
Ka-zushi Sugimoto ◽  
...  
Keyword(s):  
Hepg2 Cells ◽  
Induced Apoptosis

Induction of Apoptosis by Nano‐Synthesized Complexes of H2L and its Cu(II) Complex in Human Hepatocellular Carcinoma Cells

2020 ◽  
Vol 20 ◽  
Author(s):  
Thoria Diab ◽  
Tarek M. Mohamed ◽  
Alaa Hamed ◽  
Mohamed Gaber
Keyword(s):  
Cell Cycle ◽  
Metal Complexes ◽  
Hepg2 Cells ◽  
Therapeutic Potential ◽  
Free Ligand ◽  
Organometallic Complexes ◽  
Phase Cell ◽  
Sod Activity ◽  
Induced Apoptosis

Background: Chemotherapy is currently the most utilized treatment for cancer. Therapeutic potential of metal complexes in cancer therapy has attracted a lot of interest. The mechanisms of action of most organometallic complexes are poorly understood. Objective: This study was designed to explore the mechanisms governing the anti-proliferative effect of the free ligand N1,N6‐bis((2‐hydroxynaphthalin‐1‐yl)methinyl)) adipohydrazone (H2L) and its complexes of Mn(II), Co(II), Ni(II) and Cu(II). Methods: Cells were exposed to H2L or its metal complexes where cell viability determined by MTT assay. Cell cycle was analysed by flow cytometry. In addition, qRT-PCR was used to monitor the expression of Bax and Bcl-2. Moreover, molecular docking was carried out to find the potentiality of Cu(II) complex as an inhibitor of Adenosine Deaminase (ADA). ADA, Superoxide Dismutase (SOD) and reduced Glutathione (GSH) levels were measured in the most affected cancer cell line. Results: The obtained results demonstrated that H2L and its Cu(II) complex exhibited a strong cytotoxic activity compared to other complexes against HepG2 cells (IC50 = 4.14±0.036μM/ml and 3.2±0.02μM/ml), respectively. Both H2L and its Cu(II) complex induced G2/M phase cell cycle arrest in HepG2 cells. Additionally, they induced apoptosis in HepG2 cells via upregulation of Bax and downregulation of Bcl-2. Interestingly, the activity of ADA was decreased by 2.8 fold in HepG2 cells treated with Cu(II) complex compared to untreated cells. An increase of SOD activity and GSH level in HepG2 cells compared to control was observed. Conclusion: The results concluded that Cu(II) complex of H2L induced apoptosis in HepG2 cells. Further studies are needed to confirm its anti-cancer effect in vivo.

Role of S-adenosylhomocysteine hydrolase in adenosine-induced apoptosis in HepG2 cells

2007 ◽  
Vol 313 (2) ◽  
pp. 264-283 ◽  
Author(s):  
Marina Hermes ◽  
Hartmut Osswald ◽  
Doris Kloor
Keyword(s):  
Hepg2 Cells ◽  
Adenosylhomocysteine Hydrolase ◽  
Induced Apoptosis

Hypoxia and CoCl2 protect HepG2 cells against serum deprivation- and t-BHP-induced apoptosis: a possible anti-apoptotic role for HIF-1

2004 ◽  
Vol 295 (2) ◽  
pp. 340-349 ◽  
Author(s):  
Jean-Pascal Piret ◽  
Christophe Lecocq ◽  
Sebastien Toffoli ◽  
Noelle Ninane ◽  
Martine Raes ◽  
...  
Keyword(s):  
Hepg2 Cells ◽  
Serum Deprivation ◽  
Induced Apoptosis

Aminoguanidine Induced Apoptosis in Human Hepatocarcinoma HepG2 Cells

Gene Reports ◽  
2021 ◽  
pp. 101329
Author(s):  
Amir Najafi ◽  
Behzad Behnam ◽  
Elham jafari ◽  
Hussein Anani ◽  
Somayyeh Karami-Mohajeri
Keyword(s):  
Hepg2 Cells ◽  
Induced Apoptosis

Metallocenes-induced Apoptosis in Human Hepatic Cancer HepG2 Cells: The Prodigy of Zamzam Water

2018 ◽  
Vol 14 (2) ◽  
pp. 260-270 ◽  
Author(s):  
Ahmed Abd-Rabou ◽  
Eman Abdul-Rahm ◽  
Ramiz Saad ◽  
Hanan Sayed Ibra
Keyword(s):  
Hepg2 Cells ◽  
Hepatic Cancer ◽  
Induced Apoptosis

scholarly journals Silybin-Induced Apoptosis Occurs in Parallel to the Increase of Ceramides Synthesis and miRNAs Secretion in Human Hepatocarcinoma Cells

2019 ◽  
Vol 20 (9) ◽  
pp. 2190 ◽  
Author(s):  
Silvia Zappavigna ◽  
Daniela Vanacore ◽  
Stefania Lama ◽  
Nicoletta Potenza ◽  
Aniello Russo ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Hepg2 Cells ◽  
Thiobarbituric Acid ◽  
Strong Increase ◽  
No Production ◽  
Antiproliferative Effects ◽  
Hepatocarcinoma Cells ◽  
Induced Apoptosis ◽  
Tbars Assay ◽  
Human Hepatocarcinoma Cells

Silybin is a flavonolignan extracted from Silybum marianum (milk thistle) with hepatoprotective, antioxidant, and anti-inflammatory activity. Several studies have shown that silybin is highly effective to prevent and treat different types of cancer and that its antitumor mechanisms involve the arrest of the cell cycle and/or apoptosis. An MTT assay was performed to study cell viability, lipid peroxidation, extracellular NO production, and scavenger enzyme activity were studied by Thiobarbituric Acid-Reactive Species (TBARS) assay, NO assay, and MnSOD assay, respectively. Cell cycle and apoptosis analysis were performed by FACS. miRNA profiling were evaluated by real time PCR. In this study, we demonstrated that Silybin induced growth inhibition blocking the Hepg2 cells in G1 phase of cell cycle and activating the process of programmed cell death. Moreover, the antiproliferative effects of silybin were paralleled by a strong increase of the number of ceramides involved in the modulation of miRNA secretion. In particular, after treatment with silybin, miR223-3p and miR16-5p were upregulated, while miR-92-3p was downregulated (p < 0.05). In conclusion, our results suggest that silybin-Induced apoptosis occurs in parallel to the increase of ceramides synthesis and miRNAs secretion in HepG2 cells.

PRP1, a heteropolysaccharide from Platycodonis Radix, induced apoptosis of HepG2 cells via regulating miR-21-mediated PI3K/AKT pathway

2020 ◽  
Vol 158 ◽  
pp. 542-551
Author(s):  
Jia-Qi He ◽  
Min-Xia Zheng ◽  
Hua-Zhong Ying ◽  
Yu-Sen Zhong ◽  
Huan-Huan Zhang ◽  
...  
Keyword(s):  
Hepg2 Cells ◽  
Akt Pathway ◽  
Induced Apoptosis

scholarly journals O-GlcNAc Transferase Inhibitor Synergistically Enhances Doxorubicin-Induced Apoptosis in HepG2 Cells

Cancers ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3154
Author(s):  
Su Jin Lee ◽  
Oh-Shin Kwon
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Death ◽  
Hepg2 Cells ◽  
Drug Targets ◽  
Apoptotic Cell ◽  
Chemotherapy Resistance ◽  
Apoptotic Cell Death ◽  
Induced Apoptosis ◽  
Glcnac Transferase

The combination of chemotherapy with chemosensitizing agents is a common approach to enhance anticancer activity while reducing the dose-dependent adverse side effects of cancer treatment. Herein, we investigated doxorubicin (DOX) and O-GlcNAc transferase (OGT) inhibitor OSMI-1 combination treatment, which significantly enhanced apoptosis in hepatocellular carcinoma cells (HepG2) as a result of synergistic drug action in disparate stress signaling pathways. Treatment with a low dose of DOX or a suboptimal dose of OSMI-1 alone did not induce apoptotic cell death in HepG2 cells. However, the combination of DOX with OSMI-1 in HepG2 cells synergistically increased apoptotic cell death through the activation of both the p53 and mitochondrial Bcl2 pathways compared to DOX alone. We also demonstrated that the combination of DOX and OSMI-1 stimulated cell death, dramatically reducing cell proliferation and tumor growth in vivo using a HepG2 xenograft mouse model. These findings indicate that OSMI-1 acts as a potential chemosensitizer by enhancing DOX-induced cell death. This study provides insight into a possible mechanism of chemotherapy resistance, identifies potential novel drug targets, and suggests that OGT inhibition could be utilized in clinical applications to treat hepatocellular carcinoma as well as other cancer types.

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