Apoptotic effect of eugenol envolves G2/M phase abrogation accompanied by mitochondrial damage and clastogenic effect on cancer cell in vitro

Júnior, Paulo Luiz de Sá; Câmara, Diana Aparecida Dias; Costa, André Santos; Ruiz, Jorge L.M.; Levy, Débora; Azevedo, Ricardo A.; Pasqualoto, Kerly Fernanda Mesquita; Oliveira, Carlos; Melo, Thatiana Corrêa de; Pessoa, Nara Diniz Soares; Fonseca, Pâmela Maria Moreira; Pereira, Alexandre da Costa; Araldi, Rodrigo Pinheiro; Ferreira, Adilson Kleber

doi:10.1016/j.phymed.2016.03.014

Cited by 48 publications

(25 citation statements)

References 27 publications

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“…The analysed results show a significant increase in phosphorylated Erk1/2 after 48 and 72 h of treatment with CBE ( Figure 5A,C), as well as a time and dose-dependent increased production of ROS, lipid peroxides, and reactive nitrogen species (Figure 2). It is clear that eugenol, as part of the clove buds extract, represent a major substance associated with ROS production and lipid peroxidation [45,46]. It is also suggested that ROS can be involved also in activation of the other members of MAPK signalling including JNK and p38-MAPK [47][48][49].…”

Section: Discussionmentioning

confidence: 99%

Oxidative Stress-Induced DNA Damage and Apoptosis in Clove Buds-Treated MCF-7 Cells

et al. 2020

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In recent decades, several spices have been studied for their potential in the prevention and treatment of cancer. It is documented that spices have antioxidant, anti-inflammatory, immunomodulatory, and anticancer effects. The main mechanisms of spices action included apoptosis induction, proliferation, migration and invasion of tumour inhibition, and sensitization of tumours to radiotherapy and chemotherapy. In this study, the ability of clove buds extract (CBE) to induce oxidative stress, DNA damage, and stress/survival/apoptotic pathways modulation were analysed in MCF-7 cells. We demonstrated that CBE treatment induced intrinsic caspase-dependent cell death associated with increased oxidative stress mediated by oxygen and nitrogen radicals. We showed also the CBE-mediated release of mitochondrial pro-apoptotic factors, signalling of oxidative stress-mediated DNA damage with modulation of cell antioxidant SOD (superoxide dismutase) system, and modulation activity of the Akt, p38 MAPK, JNK and Erk 1/2 pathways.

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Section: Discussionmentioning

confidence: 99%

Oxidative Stress-Induced DNA Damage and Apoptosis in Clove Buds-Treated MCF-7 Cells

et al. 2020

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“…Eugenol inhibits the breast cancer related oncogenes, NF-κB and cyclin D1 and up-regulates the cyclin-dependent kinase inhibitor p21 WAF1 protein; On the other hand, eugenol was also cytotoxic to non-cancer cell line MCF 10A (human breast epithelial) with IC 50 value of 2.2 μM [ 50 ]. Júnior et al [ 51 ] also assessed the cytotoxicity of eugenol in the μM range on MDA-MB-231, MCF-7, SIHA (human cervix carcinoma), SK-Mel-28 (human melanoma) and A2058 (human melanoma) cells; it was accompanied by ROS production, causing G2/M phase block and, consequently, clastogenesis. Eugenol also induced downregulation of PCNA (proliferation cell nuclear antigen), decreased the mitochondria transmembrane potential and upregulated Bax [ 51 ].…”

Section: Cytotoxic and Antitumor Effects Of Eugenol And Its Relatimentioning

confidence: 99%

“…Júnior et al [ 51 ] also assessed the cytotoxicity of eugenol in the μM range on MDA-MB-231, MCF-7, SIHA (human cervix carcinoma), SK-Mel-28 (human melanoma) and A2058 (human melanoma) cells; it was accompanied by ROS production, causing G2/M phase block and, consequently, clastogenesis. Eugenol also induced downregulation of PCNA (proliferation cell nuclear antigen), decreased the mitochondria transmembrane potential and upregulated Bax [ 51 ].…”

Section: Cytotoxic and Antitumor Effects Of Eugenol And Its Relatimentioning

confidence: 99%

The Dual Antioxidant/Prooxidant Effect of Eugenol and Its Action in Cancer Development and Treatment

et al. 2017

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The formation of reactive oxygen species (ROS) during metabolism is a normal process usually compensated for by the antioxidant defense system of an organism. However, ROS can cause oxidative damage and have been proposed to be the main cause of age-related clinical complications and diseases such as cancer. In recent decades, the relationship between diet and cancer has been more studied, especially with foods containing antioxidant compounds. Eugenol is a natural compound widely found in many aromatic plant species, spices and foods and is used in cosmetics and pharmaceutical products. Eugenol has a dual effect on oxidative stress, which can action as an antioxidant or prooxidant agent. In addition, it has anti-carcinogenic, cytotoxic and antitumor properties. Considering the importance of eugenol in the area of food and human health, in this review, we discuss the role of eugenol on redox status and its potential use in the treatment and prevention of cancer.

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“…Al‐Sharif, Remmal, and Aboussekhra () displayed eugenol triggered apoptosis in breast cancer cells through E2F1/surviving down‐regulation. Junior et al () elucidated that the apoptotic effect of eugenol involved G2/M phase abrogation accompanied by mitochondrial damage and clastogenic effect on cancer cells in vitro. With respect to lung cancer, Li et al () unraveled the tumor suppressive effects of eugenol on cell proliferation, migration, and invasion partially via inhibition of PI3K/Akt pathway and MMP activity (Fangjun & Zhijia, ), However, the importance of eugenol for potential clinical applications on NSCLC was tremendously compromised due to the suspicious artifacts associated with cell culture.…”

Section: Introductionmentioning

confidence: 99%

Eugenol inhibits non‐small cell lung cancer by repressing expression of NF‐κB‐regulated TRIM59

Cui

Liu

Zeng

et al. 2019

Phytotherapy Research

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In view of the recognized anti‐tumor properties of eugenol against non‐small cell lung cancer (NSCLC) in cell culture, here we further set out to investigate the potential therapeutic effect of eugenol in vivo and elucidate the underlying molecular mechanism. The relative expression levels of TRIM59 and p65 in NSCLC were quantified by real‐time polymerase chain reaction. Xenograft tumor model was established with TRIM59‐deficient H1975 cells, and tumor progression was monitored. Kaplan–Meier's analysis was performed to measure overall survival. Protein levels of TRIM59 and p65 in xenograft tumor were determined by western blot. Direct binding of p65 on the TRIM59 promoter was analyzed by chromatin immunoprecipitation assay, and the regulatory effect was interrogated with luciferase reporter assay. Both TRIM59 and p65 were up‐regulated in NSCLC. Eugenol treatment significantly inhibited xenograft tumor progression and prolonged the overall survival of tumor‐bearing mice. Mechanistically, eugenol suppressed p65 expression, which subsequently decreased TRIM59 expression. TRIM59 deficiency fully recapitulated the anti‐tumoral phenotype elicited by eugenol. Ectopic expression of TRIM59 completely abolished the tumor suppressive effect of eugenol, which underlined the predominant role of TRIM59 in mediating the signaling downstream of eugenol treatment. Eugenol inhibited NSCLC via repression NF‐κB‐TRIM59 pathway.

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Apoptotic effect of eugenol envolves G2/M phase abrogation accompanied by mitochondrial damage and clastogenic effect on cancer cell in vitro

Abstract: These promising results presented herein shed new light on the mechanisms of action of EUG suggesting a possible applicability of this phenylpropanoid as adjuvant in anti-cancer therapy.

Cited by 48 publications

References 27 publications

Oxidative Stress-Induced DNA Damage and Apoptosis in Clove Buds-Treated MCF-7 Cells

Oxidative Stress-Induced DNA Damage and Apoptosis in Clove Buds-Treated MCF-7 Cells

The Dual Antioxidant/Prooxidant Effect of Eugenol and Its Action in Cancer Development and Treatment

Eugenol inhibits non‐small cell lung cancer by repressing expression of NF‐κB‐regulated TRIM59

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