scholarly journals Alantolactone Induces Apoptosis in HepG2 Cells through GSH Depletion, Inhibition of STAT3 Activation, and Mitochondrial Dysfunction

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Muhammad Khan ◽  
Ting Li ◽  
Muhammad Khalil Ahmad Khan ◽  
Azhar Rasul ◽  
Faisal Nawaz ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Molecular Mechanism ◽  
Hepg2 Cells ◽  
Ros Generation ◽  
Dependent Manner ◽  
Anticancer Activities ◽  
Apoptosis Resistance ◽  
Human Liver Cancer ◽  
Induced Apoptosis ◽  
Human Liver Cancer Cells

Signal transducer and activator of transcription 3 (STAT3) constitutively expresses in human liver cancer cells and has been implicated in apoptosis resistance and tumorigenesis. Alantolactone, a sesquiterpene lactone, has been shown to possess anticancer activities in various cancer cell lines. In our previous report, we showed that alantolactone induced apoptosis in U87 glioblastoma cells via GSH depletion and ROS generation. However, the molecular mechanism of GSH depletion remained unexplored. The present study was conducted to envisage the molecular mechanism of alantolactone-induced apoptosis in HepG2 cells by focusing on the molecular mechanism of GSH depletion and its effect on STAT3 activation. We found that alantolactone induced apoptosis in HepG2 cells in a dose-dependent manner. This alantolactone-induced apoptosis was found to be associated with GSH depletion, inhibition of STAT3 activation, ROS generation, mitochondrial transmembrane potential dissipation, and increased Bax/Bcl-2 ratio and caspase-3 activation. This alantolactone-induced apoptosis and GSH depletion were effectively inhibited or abrogated by a thiol antioxidant, N-acetyl-L-cysteine (NAC). The data demonstrate clearly that intracellular GSH plays a central role in alantolactone-induced apoptosis in HepG2 cells. Thus, alantolactone may become a lead chemotherapeutic candidate for the treatment of liver cancer.

scholarly journals Antiproliferative and Apoptotic Effects of Cardamonin against Hepatocellular Carcinoma HepG2 Cells

Nutrients ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1757
Author(s):  
Nassrin A. Badroon ◽  
Nazia Abdul Majid ◽  
Mohammed A. Alshawsh
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Cancer ◽  
Hepg2 Cells ◽  
Primary Liver Cancer ◽  
Dependent Manner ◽  
Anticancer Activities ◽  
Major Health Problem ◽  
Major Health ◽  
Late Apoptosis ◽  
Apoptotic Effects

Liver cancer is the sixth most common cancer in terms of incidence and the fourth in terms of mortality. Hepatocellular carcinoma (HCC) represents almost 90% of primary liver cancer and has become a major health problem globally. Cardamonin (CADMN) is a natural bioactive chalcone found in several edible plants such as cardamom and Alpinia species. Previous studies have shown that CADMN possesses anticancer activities against breast, lung, prostate and colorectal cancer. In the present study, the mechanisms underlying the anti-hepatocellular carcinoma effects of CADMN were investigated against HepG2 cells. The results demonstrated that CADMN has anti-proliferative effects and apoptotic action on HepG2 cells. CADMN showed potent cytotoxicity against HepG2 cells with an IC50 of 17.1 ± 0.592 μM at 72 h. Flow cytometry analysis demonstrated that CADMN arrests HepG2 cells in G1 phase and induces a significant increase in early and late apoptosis in a time-dependent manner. The mechanism by which CADMN induces apoptotic action was via activation of both extrinsic and intrinsic pathways. Moreover, the findings of this study showed the involvement of reactive oxygen species (ROS), which inhibit the NF-κB pathway and further enhance the apoptotic process. Together, our findings further support the potential anticancer activity of CADMN as an alternative therapeutic agent against HCC.

scholarly journals Synthesis, Characterization and Cytotoxic Studies of Benzamide Derivatives of Anacardic Acid using Human Liver Cancer Cells

2020 ◽  
pp. 1-8
Author(s):  
Dinesh Rangappa ◽  
Basappa . ◽  
Dinesh Rangappa ◽  
K.N. Thanuja ◽  
Kanchugarakoppal S. Rangappa ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Human Liver ◽  
Anacardic Acid ◽  
Anticancer Activities ◽  
Liver Cancer Cells ◽  
Human Liver Cancer ◽  
Ic50 Values ◽  
Human Liver Cancer Cells ◽  
Cytotoxic Studies

Naturally occurring anacardic acid based benzamides were reported to show anti-inflammatory and anticancer activities, where we synthesized and characterized by NMR and HRMS analysis and also tested a series of anacardic acid based benzamides and evaluated against the proliferation of human liver cancer cells (HepG2). Among the tested compounds, 6j-m showed good inhibitory activity against HepG2 cells with IC50 values ranging from 78.2-91.9 μM. In conclusion, we herein reported the newer series of an academic acid benzamides for the first time.

scholarly journals RAB9A Plays an Oncogenic Role in Human Liver Cancer Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Pengfei Sun ◽  
Lei Li ◽  
Zhongchao Li
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Hepg2 Cells ◽  
Human Liver ◽  
Apoptotic Pathway ◽  
Liver Cancer Cells ◽  
Human Liver Cancer ◽  
Hep3b Cells ◽  
Human Liver Cancer Cells

Background. RAB9, as a member of the Rab GTPase family, is required for the transport of the mannose-6-phosphate receptor (MPR) from late endosomes to trans-Golgi network (TGN). However, the role of RAB9A in tumors, including liver cancer, is still unknown. Methods. We used pcDNA3.1 plasmid to upregulate the expression of RAB9A in Hep3b cells and used specific shRNA to downregulate the expression of RAB9A in HepG2 cells. Biological functions of RAB9A were performed by CCK-8 assay, colony formation assay, apoptosis analysis, transwell assays, and wound healing assays. Finally, an in-depth mechanism study was performed by western blot. Results. RAB9A promoted the proliferation and clonality of Hep3b and HepG2 cells. RAB9A also inhibited apoptosis and the activation of mitochondrial apoptotic pathway. In addition, RAB9A promoted the invasion and migration of Hep3b and HepG2 cells. Importantly, RAB9A activated the AKT/mTOR signaling pathway in human liver cancer cells. A double-effect inhibitor (BEZ235) significantly hindered the effect of RAB9A overexpression on the proliferation and invasion of Hep3b cells. Conclusion. Our data suggest that RAB9A plays a carcinogenic role in human liver cancer progression partially through AKT signaling pathways, suggesting that RAB9A may serve as a potential therapeutic target for liver cancer therapy.

scholarly journals UHPLC-ESI-MS Analysis of Purified Flavonoids Fraction from Stem of Dendrobium denneaum Paxt. and Its Preliminary Study in Inducing Apoptosis of HepG2 Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-10
Author(s):  
Chunhua Zhou ◽  
Yingyi Luo ◽  
Zhouxi Lei ◽  
Gang Wei
Keyword(s):  
Antitumor Activity ◽  
Hepg2 Cells ◽  
High Performance ◽  
Morphological Changes ◽  
Assay Method ◽  
Ionization Mass ◽  
Dependent Manner ◽  
Esi Ms ◽  
Human Liver Cancer ◽  
Human Liver Cancer Cells

Dendrobium denneaum paxt., which has been widely used for health prevention in traditional Chinese medicine (TCM), is one of the most popular tonic herbs in China. In order to analyze its flavonoids, characterization and antitumor activity of crude extract and flavonoids rich fractions from D. denneaum paxt. were investigated. Flavonoids extracted from D. denneaum paxt. were clearly enriched in fraction II after determining the total flavonoids content; there were 15 characteristic peaks which have been detected; ultra-high performance liquid chromatography-electrospray ionization/mass spectrometry (UHPLC-ESI-MS/MS) was applied for structural elucidation of compounds. 13 characteristic peaks including flavonoid-O-glycosides and flavonoid-C-glycosides were determined or preliminarily characterized through comparing retention times and UV and MS spectra with standard compounds or documented literature. The antitumor activity of fraction II on human liver cancer cells HepG2 was investigated. MTT assay method was used to test the antiproliferation activity and to confirm the appropriate treatment concentration as well as inducing time. The morphological changes of the apoptosis cells after being induced by fraction II were observed by a Hoechst reagent and the apoptosis rate was tested by flow cytometry. The results showed that fraction II can inhibit HepG2 cells from proliferation in a dose-dependent and time-dependent manner. The apoptosis experiments indicated that fraction II can significantly induce apoptosis in HepG2 cells in a concentration over 50 μg/mL for 48 h and the most effective level was 150 μg/mL for 48 h.

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