All-trans retinoic acid and arsenic trioxide induce apoptosis and modulate intracellular concentrations of calcium in hepatocellular carcinoma cells

Wei, Jianfeng; Ye, Chao-ping; Liu, Fengsheng; Wang, Wenqing

doi:10.1179/1973947814y.0000000200

Cited by 14 publications

(11 citation statements)

References 21 publications

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“…It has also been recommended as a frontline therapy in advanced HCC by the Chinese Society of Clinical Oncology. Recent studies have demonstrated that ATO can suppress HCC cells through various mechanisms in vitro, such as suppressing proliferation [ 17 , 18 ], retarding invasion and migration [ 19 , 20 ], and reversing multidrug resistance [ 21 , 22 ]. These versatile effects imply that ATO may be suitable for the eradication of residual tumor cells.…”

Section: Introductionmentioning

confidence: 99%

Augmented EPR effect post IRFA to enhance the therapeutic efficacy of arsenic loaded ZIF-8 nanoparticles on residual HCC progression

et al. 2022

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Background Insufficient radiofrequency ablation (IRFA) can promote the local recurrence and distal metastasis of residual hepatocellular carcinoma (HCC), which makes clinical treatment extremely challenging. In this study, the malignant transition of residual tumors after IRFA was explored. Then, arsenic-loaded zeolitic imidazolate framework-8 nanoparticles (As@ZIF-8 NPs) were constructed, and their therapeutic effect on residual tumors was studied. Results Our data showed that IRFA can dramatically promote the proliferation, induce the metastasis, activate the epithelial–mesenchymal transition (EMT) and accelerate the angiogenesis of residual tumors. Interestingly, we found, for the first time, that extensive angiogenesis after IRFA can augment the enhanced permeability and retention (EPR) effect and enhance the enrichment of ZIF-8 nanocarriers in residual tumors. Encouraged by this unique finding, we successfully prepared As@ZIF-8 NPs with good biocompatibility and confirmed that they were more effective than free arsenic trioxide (ATO) in sublethal heat-induced cell proliferation suppression, apoptosis induction, cell migration and invasion inhibition, and EMT reversal in vitro. Furthermore, compared with free ATO, As@ZIF-8 NPs exhibited remarkably increased therapeutic effects by repressing residual tumor growth and metastasis in vivo. Conclusions This work provides a new paradigm for the treatment of residual HCC after IRFA. Graphical Abstract

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Section: Introductionmentioning

confidence: 99%

Augmented EPR effect post IRFA to enhance the therapeutic efficacy of arsenic loaded ZIF-8 nanoparticles on residual HCC progression

et al. 2022

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“…The natural anti-cancer compound, ATRA, has been extensively investigated for the prevention and treatment of cancer, predominantly because of its ability to induce apoptosis in cells derived from various human cancers including APL, hepatoma, breast cancer, lung cancer, and head and neck cancer [ 9 , 11 , 12 , 50 , 51 ]. The present study also showed that ATRA induced apoptosis in human hepatoma cell lines, including HepG2 and Huh7, by activating the p53-dependent apoptotic pathway.…”

Section: Discussionmentioning

confidence: 99%

Hepatitis C virus Core overcomes all-transretinoic acid-induced apoptosis in human hepatoma cells by inhibitingp14expression via DNA methylation

2017

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All-trans retinoic acid (ATRA), the most biologically active metabolite of vitamin A, is known to induce p14 expression via promoter hypomethylation to activate the p14-MDM2-p53 pathway, which leads to activation of the p53-dependent apoptotic pathway and subsequent induction of apoptosis in human hepatoma cells. In the present study, we found that hepatitis C virus (HCV) Core derived from ectopic expression or HCV infection overcomes ATRA-induced apoptosis in p53-positive hepatoma cells. For this effect, HCV Core upregulated both protein levels and enzyme activities of DNA methyltransferase 1 (DNMT1), DNMT3a, and DNMT3b and thereby repressed p14 expression via promoter hypermethylation, resulting in inactivation of the pathway leading to p53 accumulation in the presence of ATRA. As a result, HCV Core prevented ATRA from activating several apoptosis-related molecules, including Bax, p53 upregulated modulator of apoptosis, caspase-9, caspase-3, and poly (ADP-ribose) polymerase. In addition, complementation of p14 in the Core-expressing cells by either ectopic expression or treatment with 5-Aza-2′dC almost completely abolished the potential of HCV Core to suppress ATRA-induced apoptosis. Based on these observations, we conclude that HCV Core executes its oncogenic potential by suppressing the p53-dependent apoptosis induced by ATRA in human hepatoma cells.

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“…There is considerable interaction between the above compounds in cell cultures. Arsenic trioxide induced apoptosis is enhanced by ascorbate, docosahexaenoic acid, genistein, quercetin, retinoic acid (Michel et al 2003;Baumgartner et al 2004;Sanchez et al 2009;Shen et al 2012;Wei et al 2014) and ameliorated by resveratrol (Chen et al 2015). cAMP prevents apoptosis induction by palmitate, docosahexaenoic acid, arsenic trioxide and doxorubicin, in different cell lines, by promoting phosphorylation of PKA target proteins and the cAMP-GEF pathway (Kwon et al 2004;Miura et al 2005;Safa et al 2014;Fatemi et al 2015).…”

Section: Modulators Of Apoptosismentioning

confidence: 99%

Tumour initiation, store-operated calcium entry (SOCE) and apoptosis: cyclic nucleotide dependence

Williams

2020

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Chemical instigators and modulators of tumourigenesis influence cell signal transduction pathways. Cyclic nucleotides and steroid hormones may contribute to the process of carcinogenesis or provide protection via apoptotic mechanisms. Although several pharmacologic classes of compounds influence cyclic nucleotide levels markedly, less is known about the class effects of promoters and blockers of tumourigenesis and apoptosis. This molecular modeling study uses cyclic nucleotide templates to investigate relative molecular similarity within compounds modulating tumourigenesis and apoptosis. Findings, in respect of superimposition and molecular fit of the investigated compounds, are related to their individual effects on cyclic nucleotide pharmacology. Modulators of tumourigenesis and estrogen receptor sub-type ligands relate to cyclic nucleotide structure. Estradiol and GPER ligands provide a similar pattern of fit to adenine nucleotide. Chemically diverse modulators of apoptosis, including K + channel ligands, fit to different components of cyclic nucleotide structure. Compounds modulating Ca 2+ entry and IP3 receptors relate structurally to the nucleotide dioxaphosphinin moiety. Relative molecular similarity within the structures of apoptosis and tumourigenesis modulators identifies a unifying property within chemically disparate compounds. The ubiquitous generation of oxidative stress and ROS in cells by apoptosis modulating compounds may relate to the disruption of cyclic nucleotide regulated homeostasis mechanisms.

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All-trans retinoic acid and arsenic trioxide induce apoptosis and modulate intracellular concentrations of calcium in hepatocellular carcinoma cells

Cited by 14 publications

References 21 publications

Augmented EPR effect post IRFA to enhance the therapeutic efficacy of arsenic loaded ZIF-8 nanoparticles on residual HCC progression

Augmented EPR effect post IRFA to enhance the therapeutic efficacy of arsenic loaded ZIF-8 nanoparticles on residual HCC progression

Hepatitis C virus Core overcomes all-transretinoic acid-induced apoptosis in human hepatoma cells by inhibitingp14expression via DNA methylation

Tumour initiation, store-operated calcium entry (SOCE) and apoptosis: cyclic nucleotide dependence

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