scholarly journals Manilkara zapota (L.) P. Royen Leaf Water Extract Induces Apoptosis in Human Hepatocellular Carcinoma (HepG2) Cells via ERK1/2/Akt1/JNK1 Signaling Pathways

2018 ◽  
Vol 2018 ◽  
pp. 1-17 ◽  
Author(s):  
Bee Ling Tan ◽  
Mohd Esa Norhaizan ◽  
Lee Chin Chan
Keyword(s):  
Hepatocellular Carcinoma ◽  
Hepg2 Cells ◽  
Water Extract ◽  
Annexin V ◽  
Leaf Water ◽  
Human Hepatocellular Carcinoma ◽  
Enzyme Linked Immunosorbent Assay ◽  
Cytotoxicity Activity ◽  
Manilkara Zapota ◽  
Anticancer Properties

Manilkara zapota (L.) P. Royen, called sapodilla, or locally known as ciku, belongs to the family Sapotaceae. We found that Manilkara zapota leaf water extract has cytotoxic effect against human hepatocellular carcinoma (HepG2) cell line in our earlier study. Therefore, this study aimed to explore the anticancer properties of Manilkara zapota leaf water extract in HepG2 cells. We also aimed to unravel yet undiscovered mechanisms and identified several expressed genes whose functions in cytotoxicity activity of Manilkara zapota leaf water extract in HepG2 cells have not been well-studied. The apoptosis and intracellular reactive oxygen species (ROS) activities were analyzed using Annexin V-propidium iodide staining and dichlorodihydrofluorescein diacetate, respectively, by NovoCyte Flow Cytometer. Bax and Bcl-2 expression were assessed using Enzyme-Linked Immunosorbent Assay. The associated molecular pathways were evaluated by quantitative real-time PCR. Overall analyses revealed that Manilkara zapota leaf water extract can increase percentage of early apoptotic cells, induce the formation of ROS, upregulate c-Jun N-terminal kinase 1 (JNK1) and inducible nitric oxide synthase (iNOS), and reduce Akt1 and vascular endothelial growth factor A (VEGFA) transcriptional activities. Our data suggest that Manilkara zapota leaf water extract can suppress the growth of HepG2 cells via modulation of ERK1/2/Akt1/JNK1 transcriptional expression.

scholarly journals Folic acid modified TPGS as a novel nano-micelle for delivery of nitidine chloride to improve apoptosis induction in Huh7 human hepatocellular carcinoma

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Danni Li ◽  
Shaogang Liu ◽  
Jiahao Zhu ◽  
Liqun Shen ◽  
Qi ying Zhang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Folic Acid ◽  
Laser Scanning ◽  
Annexin V ◽  
Laser Scanning Confocal Microscopy ◽  
Human Hepatocellular Carcinoma ◽  
Uniform Size ◽  
Scanning Confocal Microscopy ◽  
Anticancer Properties ◽  
Huh7 Cells

Abstract Background The development of novel and effective drugs for targeted human hepatocellular carcinoma still remains a great challenge. The alkaloid nitidine chloride (NC), a component of a traditional Chinese medicine, has been shown to have anticancer properties, but doses at therapeutic levels have unacceptable side effects. Here we investigate folic acid modified D-α-tocopheryl polyethylene glycol 1000 succinate (TPGS-FA) as a potential carrier for controlled delivery of the drug. Methods Synthesized TPGS-FA was characterized by FTIR, UV-visible and 1H NMR spectroscopy, and TPGS loaded with NC was evaluated for its ability to induce apoptosis in Huh7 cells by Annexin V/PI and MTT assays, and observed by laser scanning confocal microscopy and inverted phase contrast microscopy. Results TPGS-FA/NC complexes were prepared successfully, and were homogenious with a uniform size of ~ 14 nm diameter. NC was released from the TPGS-FA/NC complexes in a controlled and sustained manner under physiological conditions (pH 7.4). Furthermore, its cytotoxicity to hepatocarcinoma cells was greater than that of free NC. Conclusions TPGS-FA is shown to be useful carrier for drugs such as NC, and TPGS-FA/NC could potentially be a potent and safe drug for the treatment of hepatocellular carcinoma.

scholarly journals Chrysophyllum cainito stem bark extract induces apoptosis in Human hepatocarcinoma HepG2 cells through ROS-mediated mitochondrial pathway

PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e10168
Author(s):  
Hau V. Doan ◽  
Pishyaporn Sritangos ◽  
Roongtip Iyara ◽  
Nuannoi Chudapongse
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Cancer ◽  
Hepg2 Cells ◽  
Primary Liver Cancer ◽  
Annexin V ◽  
Stem Bark ◽  
Human Hepatocellular Carcinoma ◽  
Bark Extract ◽  
Primary Fibroblast ◽  
Chrysophyllum Cainito

Hepatocellular carcinoma is the most common type of primary liver cancer in humans. This study aimed to demonstrate anticancer properties of an aqueous extract from Chrysophyllum cainito stem bark (CE) and its underlying mechanisms. Our MTT assay results showed that CE significantly reduced human hepatocellular carcinoma (HepG2) cell viability with the IC50of 100 µg/mL, while human dermal primary fibroblast (HDFa) cells showed less susceptibility in every concentration tested. Determined by Annexin V staining, the proportion of apoptotic HepG2 cells increased in a dose-dependent fashion after 24 hour-exposure of CE. The results from Western blot analysis confirmed that CE reduced procaspase-3, suggesting apoptosis by activating caspase-3 cleavage. Using the DCFH-DA and DiOC6 fluorescent probes, it was found that CE significantly stimulated the generation of reactive oxygen species (ROS) and reduced mitochondrial membrane potential (Δψ m), respectively. According to cell cycle analysis, CE (100 µg/mL) profoundly increased the percentage of cells in the sub-G1 phase, indicating cell apoptosis. These data suggest that CE induces apoptosis and cell death in human hepatocellular carcinoma via generation of intracellular ROS and disruption of Δψm. This is the first demonstration of the anticancer activity with proposed underlying mechanism of CE in liver cancer cells.

Ellipticine induces apoptosis through p53-dependent pathway in human hepatocellular carcinoma HepG2 cells

Life Sciences ◽  
2006 ◽  
Vol 78 (22) ◽  
pp. 2550-2557 ◽  
Author(s):  
Yu-Chun Kuo ◽  
Po-Lin Kuo ◽  
Ya-Ling Hsu ◽  
Chien-Yu Cho ◽  
Chun-Ching Lin
Keyword(s):  
Hepatocellular Carcinoma ◽  
Hepg2 Cells ◽  
Human Hepatocellular Carcinoma ◽  
Dependent Pathway

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.

scholarly journals Deoxynivalenol downregulates NRF2-induced cytoprotective response in human hepatocellular carcinoma (HepG2) cells

Toxicon ◽  
2021 ◽  
Vol 193 ◽  
pp. 4-12
Author(s):  
Siqiniseko Ndlovu ◽  
Savania Nagiah ◽  
Naeem Sheik Abdul ◽  
Terisha Ghazi ◽  
Anil A. Chuturgoon
Keyword(s):  
Hepatocellular Carcinoma ◽  
Hepg2 Cells ◽  
Human Hepatocellular Carcinoma ◽  
Cytoprotective Response

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

Fumonisin B1-induced oxidative stress triggers Nrf2-mediated antioxidant response in human hepatocellular carcinoma (HepG2) cells

2018 ◽  
Vol 35 (1) ◽  
pp. 99-109 ◽  
Author(s):  
Thilona Arumugam ◽  
Yashodani Pillay ◽  
Terisha Ghazi ◽  
Savania Nagiah ◽  
Naeem Sheik Abdul ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatocellular Carcinoma ◽  
Hepg2 Cells ◽  
Fumonisin B1 ◽  
Antioxidant Response ◽  
Human Hepatocellular Carcinoma
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