Tannic acid synergistically enhances the anticancer efficacy of cisplatin on liver cancer cells through mitochondria‑mediated apoptosis

Geng, Nana; Zheng, Xiang; Wu, Mingsong; Yang, Lei; Li, Xueying; Chen, Jindong

doi:10.3892/or.2019.7281

Cited by 19 publications

(11 citation statements)

References 32 publications

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“…The present study investigated the potential effects and mechanisms of Ta against aTo-induced cardiotoxicity. it has recently been reported that combination of Ta and antitumor agent cisplatin may exert synergistic anticancer effects and may be a novel adjuvant treatment for liver cancer (81). our next study will investigate whether Ta has synergistic or antagonistic effects when combined with aTo to treat malignant tumors.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms underlying the protective effect of tannic acid against arsenic trioxide‑induced cardiotoxicity in rats: Potential involvement of mitochondrial apoptosis

Xue

et al. 2020

Mol Med Rep

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arsenic trioxide (aTo) is a frontline chemotherapy drug used in the therapy of acute promyelocytic leukemia. However, the clinical use of aTo is hindered by its cardiotoxicity. The present study aimed to observe the potential effects and underlying mechanisms of tannic acid (Ta) against aTo-induced cardiotoxicity. Male rats were intraperitoneally injected with aTo (5 mg/kg/day) to induce cardiotoxicity. Ta (20 and 40 mg/kg/day) was administered to evaluate its cardioprotective efficacy against ATO-induced heart injury in rats. administration of aTo resulted in pathological damage in the heart and increased oxidative stress as well as levels of serum cardiac biomarkers creatine kinase and lactate dehydrogenase and the inflammatory marker NF-κB (p65). conversely, Ta markedly reversed this phenomenon. additionally, Ta treatment caused a notable decrease in the expression levels of cleaved caspase-3/caspase-3, Bax, p53 and Bad, while increasing Bcl-2 expression levels. notably, the application of Ta decreased the expression levels of cytochrome c, second mitochondria-derived activator of caspases and high-temperature requirement a2, which are apoptosis mitochondrial-associated proteins. The present findings indicated that Ta protected against aTo-induced cardiotoxicity, which may be associated with oxidative stress, inflammation and mitochondrial apoptosis.

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Section: Discussionmentioning

confidence: 99%

Mechanisms underlying the protective effect of tannic acid against arsenic trioxide‑induced cardiotoxicity in rats: Potential involvement of mitochondrial apoptosis

Xue

et al. 2020

Mol Med Rep

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“…Results revealed that TA exhibits a crucial synergistic effect with 5-FU and mitomycin C in modulating drug efflux pathways. The exact synergy was observed by combining TA and CP on HepG2 liver cancer cells through mitochondria-mediated apoptosis [ 61 ]. This chemotherapeutic sensitivity to CP was corroborated by co-treatment with procyanidins in TU686 laryngeal cancer cells through the apoptosis and autophagy pathway [ 62 ].…”

Section: Dietary Phenolic Compounds Improving the Chemosensitivity Of...mentioning

confidence: 99%

Advances in Dietary Phenolic Compounds to Improve Chemosensitivity of Anticancer Drugs

Bouyahya

Omari

Bakrim

et al. 2022

Cancers

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Despite the significant advances and mechanistic understanding of tumor processes, therapeutic agents against different types of cancer still have a high rate of recurrence associated with the development of resistance by tumor cells. This chemoresistance involves several mechanisms, including the programming of glucose metabolism, mitochondrial damage, and lysosome dysfunction. However, combining several anticancer agents can decrease resistance and increase therapeutic efficacy. Furthermore, this treatment can improve the effectiveness of chemotherapy. This work focuses on the recent advances in using natural bioactive molecules derived from phenolic compounds isolated from medicinal plants to sensitize cancer cells towards chemotherapeutic agents and their application in combination with conventional anticancer drugs. Dietary phenolic compounds such as resveratrol, gallic acid, caffeic acid, rosmarinic acid, sinapic acid, and curcumin exhibit remarkable anticancer activities through sub-cellular, cellular, and molecular mechanisms. These compounds have recently revealed their capacity to increase the sensitivity of different human cancers to the used chemotherapeutic drugs. Moreover, they can increase the effectiveness and improve the therapeutic index of some used chemotherapeutic agents. The involved mechanisms are complex and stochastic, and involve different signaling pathways in cancer checkpoints, including reactive oxygen species signaling pathways in mitochondria, autophagy-related pathways, proteasome oncogene degradation, and epigenetic perturbations.

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“…The combination of TA and cisplatin induces apoptosis in ovarian and liver cancer cells [20,21]. The binding of TA to lung uid depends on the adsorption of lung uid, which reduces the surface tension and thereby enhances the interaction between TA and lung cancer cells [22].…”

Section: Introductionmentioning

confidence: 99%

Synergistic anticancer activity of cisplatin combined with tannic acid enhances apoptosis in lung cancer through the PERK-ATF4 pathway

Zheng

Yang²,

Zhai

et al. 2022

Preprint

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Background: Cisplatin (CDDP) is a common anticancer drug whose side effects limit its clinical applications. Tannins (TA) are plant-derived polyphenols that inhibit tumor growth in different types of cancer. Here, we evaluated the anticancer effect of TA combined with CDDP on lung cancer cell lines (GLC-82 and H1299) and investigated the underlying molecular mechanism of endoplasmic reticulum (ER) stress-induced apoptosis. Methods: Cell lines were treated with CDDP, TA, and CDDP+TA, and the effect of the combination was assessed using MTT assay and observed under light and fluorescence microscopes. Cell apoptosis was detected by flow cytometry, and the expression of key factors in the ER stress apoptotic pathway was detected using qRT-PCR and western blotting. The effects of the drug combination on the tumors of nude mice injected with H1299 cells were investigated, and the expression of key factors in the ER stress apoptotic pathway was investigated. Results: The combination of CDDP and TA significantly inhibited lung cancer cell viability indicating a synergistic antitumoral effect. The mRNA and protein expression levels of key ER stress factors in the CDDP+TA group were considerably higher than those in the CDDP and TA groups, the tumor volume in tumor-bearing mice was the smallest and the number of apoptotic cells and the protein expression levels of the key ER stress in the combination group were considerably higher. Conclusions: The combination of TA and CDDP may produce synergistic antitumoral effects, mediated by the PERK-ATF4-CHOP apoptotic axis, suggesting a novel adjuvant treatment for lung cancer.

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Tannic acid synergistically enhances the anticancer efficacy of cisplatin on liver cancer cells through mitochondria‑mediated apoptosis

Cited by 19 publications

References 32 publications

Mechanisms underlying the protective effect of tannic acid against arsenic trioxide‑induced cardiotoxicity in rats: Potential involvement of mitochondrial apoptosis

Mechanisms underlying the protective effect of tannic acid against arsenic trioxide‑induced cardiotoxicity in rats: Potential involvement of mitochondrial apoptosis

Advances in Dietary Phenolic Compounds to Improve Chemosensitivity of Anticancer Drugs

Synergistic anticancer activity of cisplatin combined with tannic acid enhances apoptosis in lung cancer through the PERK-ATF4 pathway

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