Anacardic acid induces mitochondrial-mediated apoptosis in the A549 human lung adenocarcinoma cells

Seong, Yeong‐Ae; Shin, Pyung-Gyun; Kim, Gun‐Do

doi:10.3892/ijo.2013.1763

Cited by 32 publications

(21 citation statements)

References 38 publications

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“…Among them, the PERK pathway enhances translation of mRNAs, including ATF4 (Armstrong et al 2010). In a previous study, anacardic acid (6-pentadecylsalicylic acid, AA), which induced apoptosis in pituitary adenoma and lung adenocarcinoma cells through ER stress, not only significantly increased the expression of GRP78, but also increased the expression of ATF4 in both HepG2 and U266 cells (Seong et al 2013(Seong et al , 2014. IRE1 is derived from the activation of IRE.…”

Section: Discussionmentioning

confidence: 98%

Roles of oxidative stress and endoplasmic reticulum stress in selenium deficiency-induced apoptosis in chicken liver

Yao

et al. 2015

Biometals

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Oxidative stress and endoplasmic reticulum (ER) stress are involved in different types of stress-induced injuries. The aim of the present study was to evaluate the effect of Se deficiency on oxidative stress, ER stress and apoptosis in chicken livers. Chickens (1 day old, n = 180) were randomly divided into two groups: the L group [fed with a Se-deficient (Se 0.033 mg/kg) diet] and the control group [fed with a normal (Se 0.2 mg/kg) diet]. Factor-associated oxidative stress, catalase (CAT) activity, H2O2 production and the inhibition of hydroxyl radicals (·OH) in the chicken liver were determined on days 15, 25, 35, 45, 55 and 65, respectively. In addition, ER stress-related genes (GRP78, GRP94, ATF4, ATF6 and IRE) and apoptosis-related genes (caspase3 and Bcl-2) were examined by fluorescence quantitative PCR or western blot analysis. Apoptosis levels were also measured using ultrastructural observations and the TdT-mediated dUTP nick end labeling assay. The results showed that CAT activity and ·OH inhibition were decreased and that H2O2 production was increased in the low-Se group, which demonstrated that oxidative stress occurred in the chicken liver. The ER stress-related genes (GRP78, GRP94, ATF4, ATF6 and IRE) and the apoptosis-related gene caspase3 were increased (p < 0.05), while Bcl-2 was decreased (p < 0.05) by Se deficiency. In addition, apoptosis and ER lesions were observed by ultrastructural observations of the chicken liver in the low-Se group. The level of apoptosis and the number of apoptotic cells increased with time. These results indicated that the oxidative-ER stress pathway participates in Se deficiency-induced apoptosis in the chicken liver.

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Section: Discussionmentioning

confidence: 98%

Roles of oxidative stress and endoplasmic reticulum stress in selenium deficiency-induced apoptosis in chicken liver

Yao

et al. 2015

Biometals

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“…One explanation could be the improved intracellular delivery of the drug, as discussed earlier. However, the release rate seems too slow for this to be the only factor contributing to such an increase AA is a commonly acknowledged antineoplastic molecule that induces caspase-independent apoptosis 36 and inhibits the NF-κB pathway. 3 It is also an epigenetic agent that inhibits histone acetyltransferases (HATs) involved in the regulation of gene expression.…”

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confidence: 99%

Anacardic acid enhances the anticancer activity of liposomal mitoxantrone towards melanoma cell lines – in vitro studies

Legut¹,

Lipka²,

Filipczak³

et al. 2014

IJN

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This paper describes a novel formulation of antineoplastic drug: mitoxantrone loaded into liposomal carriers enriched with encapsulated anacardic acid in the liposomal bilayer using a vitamin C gradient. Anacardic acid is a potent epigenetic agent with anticancer activity. This is the first liposomal formulation to combine an actively encapsulated drug and anacardic acid. The liposomes were characterized in terms of basic parameters, such as size, zeta potential, optimal drug-to-lipid ratio, loading time and temperature, and stability at 4°C and in human plasma in vitro. The formulation was found to be stable, and the loading process was rapid and efficient (drug-to-lipid ratio of up to 0.3 with over 90% efficiency in 5 minutes). The cytotoxicity of these formulations was assessed using the human melanoma cell lines A375 and Hs294T and the normal human dermal fibroblast line. The results showed that anacardic acid and to a smaller extent vitamin C significantly increased the cytotoxicity of the drug towards melanoma compared to ammonium sulfate liposomes. On the other hand, vitamin C and anacardic acid both protected normal cells from damage caused by the drug. The formulation combining anacardic acid, vitamin C, and mitoxantrone showed promising results in terms of cytotoxicity and cytoprotection. Therefore, it has potential for anticancer treatment.

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“…Furthermore, the mediator of the intrinsic pathway involved in the release of the PARP enzyme was investigated. PARP is involved in the release of mitochondrial proteins such as cytochrome c or apoptosis-inducing factor (AIF) and regulates its translocation to the cytoplasm (19). Kenalog-IR decreased AIF protein levels in the mitochondria fraction (Fig.…”

Section: Kenalog-ir Induces Apoptosis Through the Intrinsic Mitochondmentioning

confidence: 99%

Kenalog modified by ionizing radiation induces intrinsic apoptosis mediated by elevated levels of reactive oxygen species in melanoma cancer

et al. 2018

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Kenalog is a synthetic glucocorticoid drug used to treat various cancers including ocular and choroidal melanoma. However, the drug achieves rarely sustainable results for patients. To overcome this difficulty, the structure of Kenalog was altered by ionizing radiation (IR) to develop a more effective anticancer agent for treatment of various skin cancers. The anticancer effect of modified Kenalog (Kenalog-IR) was assessed in melanoma cancer cells in vitro. The assessment of mitochondrial functions by MTT assay revealed significant inhibition of melanoma cancer cell viability by Kenalog-IR compared to Kenalog. Moreover, Kenalog-IR-induced apoptotic cell death was associated with the intrinsic mitochondrial pathway by triggering the release of intrinsic apoptosis molecules through activation of caspase-related molecules in concentration and time-dependent manners. Furthermore, it was observed that Kenalog-IR-induced apoptosis was associated with the generation of reactive oxygen species (ROS) with increased G2/M cell cycle arrest. Collectively, Kenalog-IR may be a potential suppressor of skin-related cancer in particular melanoma cancer.Abbreviations: IR, ionizing radiation; MTT, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; ROS, reactive oxygen species; IMD, incrementally modified drugs

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Anacardic acid induces mitochondrial-mediated apoptosis in the A549 human lung adenocarcinoma cells

Cited by 32 publications

References 38 publications

Roles of oxidative stress and endoplasmic reticulum stress in selenium deficiency-induced apoptosis in chicken liver

Roles of oxidative stress and endoplasmic reticulum stress in selenium deficiency-induced apoptosis in chicken liver

Anacardic acid enhances the anticancer activity of liposomal mitoxantrone towards melanoma cell lines – in vitro studies

Kenalog modified by ionizing radiation induces intrinsic apoptosis mediated by elevated levels of reactive oxygen species in melanoma cancer

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Anacardic acid induces mitochondrial-mediated apoptosis in the A549 human lung adenocarcinoma cells

Cited by 32 publications

References 38 publications

Roles of oxidative stress and endoplasmic reticulum stress in selenium deficiency-induced apoptosis in chicken liver

Roles of oxidative stress and endoplasmic reticulum stress in selenium deficiency-induced apoptosis in chicken liver

Anacardic acid enhances the anticancer activity of liposomal mitoxantrone towards melanoma cell lines &ndash; in vitro studies

Kenalog modified by ionizing radiation induces intrinsic apoptosis mediated by elevated levels of reactive oxygen species in melanoma cancer

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Anacardic acid enhances the anticancer activity of liposomal mitoxantrone towards melanoma cell lines – in vitro studies