Multifunctional selenium nanoparticles with Galangin-induced HepG2 cell apoptosis through p38 and AKT signalling pathway

The morbidity and mortality of hepatocellular carcinoma, the most common cancer, are increasing continuously worldwide. Galangin (Ga) has been demonstrated to possess anti-cancer effect, but the efficacy of Ga was limited by its low permeability and poor solubility. To develop aqueous formulation and improve the anti-cancer activity of Ga, surface decoration of functionalized selenium nanoparticles with Ga (Se@Ga) was synthesized in the present study. The aim of this study was to evaluate the anti-cancer effect of Se@Ga and the mechanism on HepG2 cells. Se@Ga-induced HepG2 cell apoptosis was confirmed by depletion of mitochondrial membrane potential, translocation of phosphatidylserine and caspase-3 activation. Furthermore, Se@Ga enhanced the anti-cancer activity of HepG2 cells through ROS-mediated AKT and p38 signalling pathways. In summary, these results suggest that Se@Ga might be potential candidate chemotherapy for cancer.

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Surface decoration of selenium nanoparticles with curcumin induced HepG2 cell apoptosis through ROS mediated p53 and AKT signaling pathways

RSC Advances ◽

10.1039/c7ra08796a ◽

2017 ◽

Vol 7 (83) ◽

pp. 52456-52464 ◽

Cited By ~ 21

Author(s):

Min Guo ◽

Yinghua Li ◽

Zhengfang Lin ◽

Mingqi Zhao ◽

Misi Xiao ◽

...

Keyword(s):

Signaling Pathways ◽

Hepg2 Cell ◽

Cell Apoptosis ◽

Akt Signaling ◽

Selenium Nanoparticles ◽

Apoptotic Signaling ◽

Surface Decoration

Curcumin surface decorated selenium nanoparticles (Se@Cur) has been described in this study. The apoptotic signaling pathways triggered by the Se@Cur are p53 and AKT pathways.

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Kaempferol inhibits proliferation, migration, and invasion of liver cancer HepG2 cells by down-regulation of microRNA-21

International Journal of Immunopathology and Pharmacology ◽

10.1177/2058738418814341 ◽

2018 ◽

Vol 32 ◽

pp. 205873841881434 ◽

Cited By ~ 14

Author(s):

Genglong Zhu ◽

Xialei Liu ◽

Haijing Li ◽

Yang Yan ◽

Xiaopeng Hong ◽

...

Keyword(s):

Cell Proliferation ◽

Liver Cancer ◽

Signaling Pathway ◽

Hepg2 Cell ◽

Cell Apoptosis ◽

Hepg2 Cells ◽

Mtor Signaling ◽

Brdu Incorporation ◽

Migration And Invasion ◽

Mtor Signaling Pathway

Liver cancer is one of the most common and lethal cancers in human digestive system, which kills more than half a million people every year worldwide. This study aimed to investigate the effects of kaempferol, a flavonoid compound isolated from vegetables and fruits, on hepatic cancer HepG2 cell proliferation, migration, invasion, and apoptosis, as well as microRNA-21 (miR-21) expression. Cell viability was detected using cell counting kit-8 (CCK-8) assay. Cell proliferation was measured using 5-bromo-2′-deoxyuridine (BrdU) incorporation assay. Cell apoptosis was assessed using Guava Nexin assay. Cell migration and invasion were determined using two-chamber migration (invasion) assay. Cell transfection was used to change the expression of miR-21. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was performed to analyze the expressions of miR-21 and phosphatase and tensin homologue (PTEN). Expression of key proteins involved in proliferation, apoptosis, migration, invasion, and phosphatidylinositol 3-kinase/protein kinase 3/mammalian target of rapamycin (PI3K/AKT/mTOR) pathway were evaluated using western blotting. Results showed that kaempferol significantly inhibited HepG2 cell proliferation, migration, and invasion, and induced cell apoptosis. Kaempferol remarkably reduce the expression of miR-21 in HepG2 cells. Overexpression of miR-21 obviously reversed the effects of kaempferol on HepG2 cell proliferation, migration, invasion, and apoptosis. Moreover, miR-21 negatively regulated the expression of PTEN in HepG2 cells. Kaempferol enhanced the expression of PTEN and inactivated PI3K/AKT/mTOR signaling pathway in HepG2 cells. In conclusion, kaempferol inhibited proliferation, migration, and invasion of HepG2 cells by down-regulating miR-21 and up-regulating PTEN, as well as inactivating PI3K/AKT/mTOR signaling pathway.

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(−)-Epigallocatechin-3-Gallate (EGCG), Green Tea Component, Antagonize the Anti-Myeloma Activity of Proteasome Inhibitor PS-341 by Direct Chemical Interaction.

Blood ◽

10.1182/blood.v110.11.4850.4850 ◽

2007 ◽

Vol 110 (11) ◽

pp. 4850-4850 ◽

Cited By ~ 1

Author(s):

Tae Young Kim ◽

Jongmin Park ◽

Bora Oh ◽

Hyun Jung Min ◽

Tae-Sook Jeong ◽

...

Keyword(s):

Synergistic Effect ◽

Boronic Acid ◽

Chemical Interaction ◽

Chemotherapeutic Agents ◽

Antagonistic Effect ◽

Potential Candidate ◽

Myeloma Cells ◽

Anti Cancer ◽

Antioxidant Function ◽

Cancer Activity

Abstract PS-341 (also known as bortezomib, Velcade®) has a remarkable anti-myeloma acitivity and is also potential candidate for the treatment of other tumors either alone or in combination with other chemotherapeutic agents. Investigations on the effectiveness of PS-341 in combination with other anti-neoplastic agents are currently under clinical trial. Since (−)-epigallocatechin-3-gallate (EGCG) has been reported its anti-cancer activity in various cancer types, we tried a co-treatment of PS-341 with EGCG on myeloma cells, expecting a synergistic effect. However, the anti-cancer activity of PS-341 was blocked by EGCG without any synergistic effect. At the early stage of our research, we suspected antioxidant function of EGCG is the main cause of antagonistic effect on PS-341-induced cell death. Thus we selected polyphenols showing strong antioxidant function including vitamin C. But, we did not obtain any consistant data that support the significant correlation of antioxidant function of polyphenols with antagonistic effects. Instead, the structural features of polyphenols showed striking correlations with antagonistic effect; especially the presence or absence of vicinal diol moiety on polyphenol was the key elements for the effective blocking on anti-cancer function of PS-341. We infer that vicinal diols on polyphenols interact with boronic acid of PS-341, which convert active triangular boronic acid (sp2 character) of PS-341 to inactive tetrahedral boronate (sp3 character) through direct chemical interaction. The equilibrium of this conversion is controlled by structures and concentration of polyphenols, and this conversion abolished the anti-myeloma activity of PS-341. We confirmed our hypothesis on direct chemical interaction of PS-341 with EGCG through 11B NMR experiment and cell viability assay data clearly support the antagonistic interaction between PS-341 and polyphenols in multiple myeloma cell lines and primary myeloma cells from patients. Based on our researches, restriction of the intake of natural polyphenols by food or vitamin supplements should be considered during the treatment with PS-341 in MM patients. Figure Figure

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Effect of Juglone on Migration of Human Ovarian Cancer SKOV3 Cells

Advanced Materials Research ◽

10.4028/www.scientific.net/amr.912-914.1911 ◽

2014 ◽

Vol 912-914 ◽

pp. 1911-1914

Author(s):

Liang Zhong Zhao ◽

Shuang Chen ◽

Qing Fang ◽

Duo Zhang ◽

You Peng Zhu ◽

...

Keyword(s):

Ovarian Cancer ◽

Wound Healing ◽

Plant Species ◽

Human Ovarian Cancer ◽

Skov3 Cell ◽

Potential Candidate ◽

Wound Healing Assay ◽

Skov3 Cells ◽

Anti Cancer ◽

Cancer Activity

Juglone is isolated from many plant species belonging to Juglandaceae family. Recent studies have shown that Juglone exhibits various bioactivities including anti-tumor functions. However, its anti-cancer activity on human ovarian cancer SKOV3 cell has not been examined. Thus, the current study was designed to elucidate the effect of Juglone on migration of human ovarian cancer SKOV3 cells. In the present study, SKOV3 cells were incubated with Juglone at various concentrations. Wound healing assay and Transwell chambers were used to detect migration of SKOV3 treated with Juglone for 24h. The result showed that Juglone inhibited the migration of SKOV3 cells with concentration of Juglone at 25, 50 or 100μM compared with control cells. Therefore, our results indicated that Juglone may be a potential candidate of drug for ovarian cancer.

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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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FAK and S6K1 Inhibitor, Neferine, Dually Induces Autophagy and Apoptosis in Human Neuroblastoma Cells

Molecules ◽

10.3390/molecules23123110 ◽

2018 ◽

Vol 23 (12) ◽

pp. 3110 ◽

Cited By ~ 12

Author(s):

Dinh-Chuong Pham ◽

Yu-Chuan Chang ◽

Shian-Ren Lin ◽

Yuh-Ming Fuh ◽

May-Jywan Tsai ◽

...

Keyword(s):

Cell Migration ◽

Cancer Cells ◽

Molecular Mechanisms ◽

Caspase 3 ◽

Neuroblastoma Cells ◽

Beclin 1 ◽

Potential Candidate ◽

Human Neuroblastoma Cells ◽

Human Neuroblastoma ◽

Anti Cancer

Human neuroblastoma cancer is the most typical extracranial solid tumor. Yet, new remedial treatment therapies are demanded to overcome its sluggish survival rate. Neferine, isolated from the lotus embryos, inhibits the proliferation of various cancer cells. This study aimed to evaluate the anti-cancer activity of neferine in IMR32 human neuroblastoma cells and to expose the concealable molecular mechanisms. IMR32 cells were treated with different concentrations of neferine, followed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay to assess cell viability. In an effort to determine the molecular mechanisms in neferine-incubated IMR32 cells, cell cycle arrest, cell migration, and focal adhesion kinase (FAK), the 70-kDa ribosomal S6 kinase 1 (S6K1), poly (ADP-ribose) polymerase (PARP), caspase-3, Beclin-1, and microtubule-associated protein 1A/1B-light chain 3 (LC3) protein expressions were investigated. Neferine strongly disrupted the neuroblastoma cell growth via induction of G2/M phase arrest. Furthermore, neferine provoked autophagy and apoptosis in IMR32 cells, confirmed by p-FAK, and p-S6K1 reduction, LC3-II accumulation, Beclin-1 overexpression, and cleaved caspase-3/PARP improvement. Finally, neferine markedly retarded cell migration of neuroblastoma cancer cells. As a result, our findings for the first time showed an explicit anti-cancer effect of neferine in IMR32 cells, suggesting that neferine might be a potential candidate against human neuroblastoma cells to improve clinical outcomes with further in vivo investigation.

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IN VIVO AND IN VITRO EVALUATION OF ANTI-CANCER ACTIVITY OF NEWLY SYNTHESIZED COBALT COMPLEX OF COUMARIN SCHIFF BASES

INDIAN DRUGS ◽

10.53879/id.54.04.10792 ◽

2017 ◽

Vol 54 (04) ◽

pp. 61-69

Author(s):

A. Rayaji ◽

A. H. M. Viswanatha Swamy ◽

Keyword(s):

Nitric Oxide ◽

Hepg2 Cell ◽

Cobalt Complex ◽

Reducing Ability ◽

Anti Cancer ◽

Anti Oxidant ◽

Hepg2 Cell Lines ◽

Cancer Activity

Hepatocarcinogenesis is a multistep process involving different genetic alterations that ultimately lead to malignant transformation of the hepatocytes. Modern treatment of cancer includes chemotherapy, hormone therapy, radiotherapy and surgery but they are associated with several adverse effects such as alopecia, fatigue and general weakening of the body’s immune system due to bone marrow suppression. However, there is a continual need to look out for newer drugs to overcome the menace of cancer. In view of this we synthesized the new Coumarin-Cobalt complex derivatives. Structures of all the newly synthesized metal complexes are supported by Spectral data such as IR, NMR, and mass spectrometry. Coumarin-Cobalt complex of vanillin exhibited significant anti-cancer activity by in vivo anticancer activity (BrdU estimation). Immunohistochemical analysis has been done by BrdU and the synthesized compounds were screened for anti-oxidant activity and in vitro HepG2 cell lines. The IC50 values of the HepG2 cell lines as compared with that of standard Cisplatin and compounds IIIb, IIId, IIIe, IIIh and IIIj showed appreciable activity at a concentration less than 10 μG. Coumarin-Cobalt complex of vanillin exhibited significant anti-cancer activity. Anti-oxidant activity performed by Nitric oxide reducing ability, Superoxide dismutase and reducing activity:Compounds IIIc, IIIe and IIIg showed appreciable activity at 400μg/mL and 800 μg/mL screened by nitric oxide reducing ability, superoxide anion was effectively scavenged by compound IIIg at 400μg/mL and 800 μg/mL and reducing power of compounds IIIc and IIIj is comparable with standard ascorbic acid at concentrations 400μg/mL and 800 μg/mL.

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Taraxerol protects the human hepatic L02 cells from hydrogen peroxide-induced apoptosis

Bangladesh Journal of Pharmacology ◽

10.3329/bjp.v12i2.30985 ◽

2017 ◽

Vol 12 (2) ◽

pp. 20 ◽

Cited By ~ 1

Author(s):

Xiang-Yang Yao ◽

Qin Bai

Keyword(s):

Oxidative Stress ◽

Hydrogen Peroxide ◽

Caspase 3 ◽

Protective Agent ◽

Cytoprotective Effect ◽

Lactate Dehydrogenase Release ◽

Anti Cancer ◽

Induced Apoptosis ◽

L02 Cells ◽

Cancer Activity

Taraxerol is known to exhibit anti-inflammatory and anti-cancer activity. However, cytoprotective effect of taraxerol on hepatocytes has not been reported. In the present study, we investigated the hepatoprotective effect of taraxerol in the human hepatic L02 cells injured by hydrogen peroxide (H2O2). Taraxerol decreased H2O2-induced cell viability loss and lactate dehydrogenase release. Taraxerol also inhibited H2O2-induced cell apoptosis. Further, taraxerol attenuated H2O2-induced increase in cleaved-caspase-3 and cleaved-PARP. H2O2-activated p38 and JNK were also inhibited by taraxerol. These data suggest that taraxerol could protect the L02 cells against H2O2-induced apoptosis via suppression of p38 and JNK. Taraxerol may be an effective protective agent against oxidative stress-induced liver injury.

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Identification of acetylshikonin as the novel CYP2J2 inhibitor with anti-cancer activity in HepG2 cells

Phytomedicine ◽

10.1016/j.phymed.2016.12.001 ◽

2017 ◽

Vol 24 ◽

pp. 134-140 ◽

Cited By ~ 17

Author(s):

See-Hyoung Park ◽

Nguyen Minh Phuc ◽

Jongsung Lee ◽

Zhexue Wu ◽

Jieun Kim ◽

...

Keyword(s):

Hepg2 Cells ◽

The Novel ◽

Anti Cancer ◽

Cancer Activity

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Protective Effect of Two Alkaloids from Hippophae rhamnoides Linn. against Doxorubicin-Induced Toxicity in H9c2 Cardiomyoblasts

Molecules ◽

10.3390/molecules26071946 ◽

2021 ◽

Vol 26 (7) ◽

pp. 1946

Author(s):

Wenna Zhou ◽

Jian Ouyang ◽

Na Hu ◽

Gang Li ◽

Honglun Wang

Keyword(s):

Protein Expression ◽

Protective Effect ◽

Caspase 3 ◽

Cardiac Cells ◽

Potential Candidate ◽

H9c2 Cells ◽

Cardiac Muscle Cells ◽

Anti Cancer ◽

H9c2 Cardiomyoblasts ◽

Induced Apoptosis

Background: Doxorubicin (Dox) is one of the most frequently prescribed anti-cancer drugs. However, clinical application with Dox is limited due to its potentially fatal cumulative cardiotoxicity. N-p-coumaroyl-4-aminobutan-1-ol (alk-A), an organic amide alkaloid and hippophamide (alk-B), a rare pyridoindole alkaloid were successfully obtained by purification and separation of seabuckthorn seed residue in our previous research. This study was undertaken to investigate the protective effect of alk-A and alk-B against Dox-induced embryonic rat cardiac cells (H9c2 cells) apoptosis. Methods: H9c2 cells were treated with Dox (2.5 µM) in the presence of alk-A and alk-B (10, 20, and 40 µM) and incubated for 24 h. Results: It was shown that pretreatment of the H9c2 cells with alk-A and alk-B significantly reduced Dox-induced apoptosis. Alk-A and alk-B both inhibited reactive oxygen species (ROS) production and suppressed cleaved-caspase-3 protein expression and the activation of JNK (Jun N-terminal kinases), as well as increasing ATP levels, favoring mitochondrial mitofusin protein expression, and relieving damage to mitochondrial DNA. Conclusions: These results suggest that alk-A and alk-B can inhibit Dox-induced apoptosis in H9C2 cardiac muscle cells via inhibition of cell apoptosis and improvement of mitochondrial function, while alk-B showed more protection. Alk-B could be a potential candidate agent for protecting against cardiotoxicity in Dox-exposed patients.

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