Cytotoxicity of Ethyl Acetate Extract From Broussonetia luzonica (Moraceae) Blanco Leaves against Hepatocellular Carcinoma (Hepg2) Cell Lines

Background: Silver nanoparticles play a significant role in bioavailability and refining the compatibility of natural drugs in the treatment of various chronic diseases including different types of cancer. Objective: Green synthesis of silver nanocomposites of Nigella sativa seeds extract to evaluate the anticancer effects against hepatocellular carcinoma using HepG2 cell lines. Methods: The AgNCs were developed by treating aqueous extract of N. sativa seeds treated with silver nitrate (1mM) solution and were used to test its efficacy against hepatocellular carcinoma using HepG2 cell lines. Results and Discussion: The Surface Plasmon Resonance (SPR) of prepared AgNCs showed a peak at 432 nm via UV spectroscopy. The selected N. sativa AgNCs were characterized for polydispersity, surface charge and size and the results showed 0.215±0.093 polydispersity index (PDI), zeta potential 18.8±0.372 mV and size range 10-20 nm, respectively. The Fourier transform infrared spectroscopy (FTIR) also showed various peak of functional groups that are possibly involved in the reduction of silver ion and synthesized the N. sativa silver nanocomposites, respectively. N. sativa AgNCs showed 89.954% drug release while in the case of extract release, it was only 33.821% in 24 hrs. Further, in vitro studies of N. sativa AgNCs against hepatocellular carcinoma showed good cytotoxic effect p<0.05 with 7.16 µg/ml IC50 value. Conclusion: Thus, the present results revealed that green synthesis of N. sativa AgNCs can be an alternative tool for clinical application in cancer therapy; however, there is a need to find the mechanism and role of AgNCs inside the individual.

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ID: 1085 Sodium citrate induces apoptosis in HepG2 cell lines

Biomedical Research and Therapy ◽

10.15419/bmrat.v4is.359 ◽

2017 ◽

Vol 4 (S) ◽

pp. 174

Author(s):

Sinh Truong Nguyen ◽

Phuc Hong Vo ◽

Oanh Thi-Kieu Nguyen ◽

Nghia Minh Do ◽

Phuc Van Pham

Keyword(s):

Hepatocellular Carcinoma ◽

Cancer Cells ◽

Dna Fragmentation ◽

Hepg2 Cell ◽

Cell Lines ◽

Hepg2 Cells ◽

Caspase 3 ◽

Sodium Citrate ◽

Dependent Manner ◽

Hepg2 Cell Lines

PURPOSES: Cancer cells were observed to increase glucose uptake and fermentation of glucose to lactate to to synthesis rapidly ATP for cell growth, survival and proliferation. Thus, inhibition of glycolysis might be useful in antitumor treatment. This phenomenon occurred even with fully functioning mitochondria, and known as Warberg effect. Sodium citrate, an inhibitor of Warberg effect, was reported to antiproliferate many cancer cells line. However, sodium citrate has not been studied in Hepatocellular Carcinoma cells line yet. Here we aimed to investigate the effect of sodium citrate in HepG2 cells line. MATERIAL AND METHODS: HepG2 cell lines was treated with sodium citrate at different concentrations. Viable cells were determined by Alamar Blue. The apoptosis induced-cells was detected by Annexin V with FCM technique. Disintegrated nuclei and DNA fragmentation was analyzed. The activity of caspase-3 was also tested. RESULTS: We observed that the IC50 value of sodium citrate on HepG2 is at 10mM. FCM analysis showed that sodium citrate induced apoptosis in HepG2 cell line in dose-dependent manner. At 10mM sodium citrate, the caspase-3/7 was observed to be activated in time-dependent manner. Sodium citrate also induced nuclei disintergated in HepG2. DNA fragmentation was observed when HepG2 cells were treated with 10mM sodium citrate. CONCLUSIONS: We have shown that sodium citrate possesses the antiproliferative ability on HepG2 at IC50 10mM. Sodidum citrate induces apoptosis cells in hepatocellular carcinoma HepG2 by capases-3 activation. More investigation of glycolysis inhibition of sodium citrate on HepG2 should be performed in animals

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Evaluation of the Consequence of CTNNB1 & RAB1A Targeting on Hepatocellular Carcinoma Cell Line

QJM ◽

10.1093/qjmed/hcab088.001 ◽

2021 ◽

Vol 114 (Supplement_1) ◽

Author(s):

Amira Salah Ismail ◽

Samar Kamal Kassim ◽

Hanan H Shehata ◽

Magda I Mohamad ◽

Marian Maher Salib Roushdy

Keyword(s):

Hepatocellular Carcinoma ◽

Cell Proliferation ◽

Liver Cancer ◽

Hepg2 Cell ◽

Cell Lines ◽

Hepg2 Cells ◽

Proliferative Activity ◽

Trypan Blue ◽

Liver Tumors ◽

Hepg2 Cell Lines

Abstract Background Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer in adults and the most common cause of death in people with chronic liver diseases. In Egypt, liver cancer forms 11.75% of the malignancies of all digestive organs and 1.68% of the total malignancies. HCC constitutes 70.48% of all liver tumors among Egyptians. In the past few years, early diagnosis and advances in therapeutic measures have greatly improved the outcome of HCC patients. However, the prognosis is still poor with overall survival rates of 3-5%. The alterations in cancer driver genes and associated pathways are the major triggers for HCC. So, the identification and targeting of these genes are beneficial to understand HCC and to develop a new therapy. Aim of the work We aimed to target CTNNB1 and RAB1A oncogenes in HepG2 cell lines by RNAi then evaluate the effect of their targeting on the viability and proliferative activity of HepG2 cells. Materials and methods Using HepG2 cell lines, CTNNB1 & RAB1A oncogenes were targeted using two different siRNAs (small interfering RNA) for each gene. The viability of HepG2 was conducted by Trypan blue test. The cell proliferation was tested by CellTiter 96® AQueous One Solution Cell Proliferation Assay. Results There was significant reduction in the cells’ viability detected by trypan blue test in transfected cells with siRNA targeting either CTNNB1 or RAB1A compared to Mock HepG2 cell lines (p <0.05). In addition, the proliferative activity was significantly lower in both HepG2 cell lines transfected with siRNA targeting the previous genes compared to mock cells (p < 0.05). Furthermore, HepG2 cells transfected with siRNA targeting RAB1A were more proliferative compared to those transfected with siRNA targeting CTNNB1 (p <0.05). Conclusion Targeting CTNNB1or RAB1A in HepG2 cell lines decreased the cell viability and proliferative activity. Moreover, targeting CTNNB1 was effective in decreasing cell proliferative activity compared to targeting RAB1A in HepG2 cell lines. So, targeting CTNNB1 may have a potential therapeutic effect in treatment of HCC.

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Antiproliferation and apoptosis induction of phytic acid in hepatocellular carcinoma (HEPG2) cell lines

AFRICAN JOURNAL OF BIOTECHNOLOGY ◽

10.5897/ajb11.699 ◽

2011 ◽

Vol 10 (73) ◽

Cited By ~ 3

Author(s):

Saad Norazalina

Keyword(s):

Hepatocellular Carcinoma ◽

Phytic Acid ◽

Hepg2 Cell ◽

Cell Lines ◽

Apoptosis Induction ◽

Hepg2 Cell Lines

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Sawtehtetronenin from Goniothalamus sawtehii and its Cytotoxicity

Natural Product Communications ◽

10.1177/1934578x1400901228 ◽

2014 ◽

Vol 9 (12) ◽

pp. 1934578X1400901

Author(s):

Chiarpha Thiplueang ◽

Sittiporn Punyanitya ◽

Ratana Banjerdpongchai ◽

Benjawan Wudtiwai ◽

Phansuang Udomputtimekakul ◽

...

Keyword(s):

Breast Cancer ◽

Hepatocellular Carcinoma ◽

Ethyl Acetate ◽

Cell Lines ◽

Ethyl Acetate Extract ◽

Human Hepatocellular Carcinoma ◽

Chemotherapeutic Drug ◽

Spectral Evidence ◽

Related Compounds ◽

C Nmr

A new acetogenin has been isolated from the ethyl acetate extract of leaves and twigs of G. sawtehii (Annonaceae). The structure of compound 1 was identified as sawtehtetronenin on the basis of spectral evidence (UV, IR, MS and 1H, and 13C NMR) and by comparison with related compounds. Sawtehtetronenin was found to be cytotoxic to human hepatocellular carcinoma HepG2 and breast cancer MDA-MB231 cells with IC50 values of 79.3+11.9 μM and 108.1+1.5 μM, respectively. Compound 1 was less toxic to both cell lines when compared with camptothecin, a chemotherapeutic drug.

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Anticancer Effect of Amygdalin (Vitamin B-17) on Hepatocellular Carcinoma Cell Line (HepG2) in the Presence and Absence of Zinc

Anti-Cancer Agents in Medicinal Chemistry ◽

10.2174/1871520620666200120095525 ◽

2020 ◽

Vol 20 (4) ◽

pp. 486-494

Author(s):

Mohamed A. El-Desouky ◽

Abdelgawad A. Fahmi ◽

Ibrahim Y. Abdelkader ◽

Karima M. Nasraldin

Keyword(s):

Hepatocellular Carcinoma ◽

Cell Cycle ◽

Cytochrome C ◽

Cell Cycle Arrest ◽

Cell Line ◽

Hepg2 Cell ◽

Caspase 3 ◽

Vitamin B ◽

Cycle Arrest ◽

Hepg2 Cell Lines

Background: Amygdalin (Vitamin B-17) is a naturally occurring vitamin found in the seeds of the fruits of Prunus Rosacea family including apricot, bitter almond, cherry, and peach. Objective: The purpose of this study was to examine the effect of amygdalin with and without zinc on hepatocellular carcinoma (HepG2) cell line. Methods: MTT assay was used to evaluate the cytotoxicity of amygdalin without zinc, amygdalin + 20μmol zinc, and amygdalin + 800μmol zinc on HepG2 cell lines. The cell cycle distribution assay was determined by flow cytometry. Apoptosis was confirmed by Annexin V-FITC/PI staining assay. Moreover, the pathway of apoptosis was determined by the percentage of change in the mean levels of P53, Bcl2, Bax, cytochrome c, and caspase-3. Results: Amygdalin without zinc showed strong anti-HepG2 activity. Furthermore, HepG2 cell lines treatment with amygdalin + 20μmol zinc and amygdalin + 800μmol zinc showed a highly significant apoptotic effect than the effect of amygdalin without zinc. Amygdalin treatment induced cell cycle arrest at G2/M and increased the levels of P53, Bax, cytochrome c, and caspase-3 significantly, while it decreased the level of anti-apoptotic Bcl2. Conclusion: Amygdalin is a natural anti-cancer agent, which can be used for the treatment of hepatocellular carcinoma. It promotes apoptosis via the intrinsic cell death pathway (the mitochondria-initiated pathway) and cell cycle arrest at G/M. The potency of amygdalin in HepG2 treatment increased significantly by the addition of zinc.

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