Autophagic Cell Death Is Induced by Acetone and Ethyl Acetate Extracts from<i>Eupatorium odoratum In Vitro</i>: Effects on MCF-7 and Vero Cell Lines

Harun, Faizah Bt.; Jamalullail, Syed Mohsin Syed Sahil; Khoo, Boon Yin; Othman, Zulkhairi; Tilwari, Anita; Balaram, Prabha

doi:10.1100/2012/439479

Cited by 21 publications

(21 citation statements)

References 28 publications

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“…We observed an increase in LC3B-II expression in cells treated with the seed extract. Other researchers also observed autophagy caused by plant extracts treatments on MCF-7 cells [27,28]. Ait-Mohamed et al [27] observed that acetonic extract of Buxus sempervirens induced autophagy in MCF-7 cells.…”

Section: Discussionmentioning

confidence: 97%

Cytotoxic effects of Euterpe oleracea Mart. in malignant cell lines

Silva

Vidal

Santos

et al. 2014

BMC Complement Altern Med

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BackgroundEuterpe oleracea Mart., a plant from the Amazon region, is commonly known as açaí or juçara; it has high nutritional value and elevated levels of lipids, proteins, and minerals. Açaí is an abundant and much consumed fruit by the Amazon local population, and studies have demonstrated that it is rich in phytochemicals with antioxidant, anti-inflammatory, and anticancer activities. Therefore, the aim of this study was to test this plant for anticancer activity in different human malignant cell lines.MethodsCell lines derived from breast and colorectal adenocarcinomas were treated with 10, 20, and 40 μg/mL of bark, seed, and total açaí fruit hydroalcoholic extracts for 24 and 48 h. After treatment, cell viability was measured using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays, and cell morphological features were observed by light and transmission electron microscopy. The type of cell death was also evaluated. The data were analyzed statistically by one-way analysis of variance (ANOVA), followed by Dunnett’s or Tukey’s post hoc tests, as appropriate.ResultsWe observed that of all the cell lines tested, MCF-7 was the only line that responded to açaí treatment. The extracts caused significant reduction (p < 0.01) in cell viability and altered cell morphological features by inducing the appearance of autophagic vacuoles, as observed by transmission electron microscopy. Furthermore, increased expression of LC3BII, a protein marker of autophagosome formation, was observed by western blotting. Caspase Glo™ assays and morphologic observations by DAPI nuclear staining and transmission electron microscopy did not indicate any apoptotic events.ConclusionsThe present study demonstrated that açaí possesses antitumorigenic potential in the MCF-7 cell line. Further studies are needed to identify the compound (s) responsible for this cytotoxic activity and the molecular target in the cell. This discovery of the anticancer potential of açaí may help in the development of chemopreventive drugs and may have therapeutic effects in the treatment of breast cancer.

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Section: Discussionmentioning

confidence: 97%

Cytotoxic effects of Euterpe oleracea Mart. in malignant cell lines

Silva

Vidal

Santos

et al. 2014

BMC Complement Altern Med

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“…Currently, the effects of autophagy in neurodevelopment have attracted more attention. Ding et al found the expression of autophagy‐related molecule Beclin1 was reduced in 44 hepatocellular carcinoma patients, indicating that autophagy could inhibit the process of tumor differentiation; Harun et al revealed that acetone and ethyl acetate extracts from Eupatorium odoratum could induce autophagic cell death in MCF‐7 and Vero cell lines; and Chatterjee et al found that a low concentration of mercury induces autophagic cell death in rat hepatocytes. As a widely used autophagy inhibitor, 3MA can inhibit autophagosome formation by interfering with the activity of VPS34, which is a component of the Beclin1‐PI3KC3 complex .…”

Section: Discussionmentioning

confidence: 99%

Oxidative stress‐mediated autophagic cell death participates in the neurotoxic effect on SH‐SY5Y cells induced by excessive iodide

Liu

Wang

Zeng

et al. 2018

Environmental Toxicology

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Excessive iodide could induce intellectual damage in children, which has attracted broad attention. To investigate the neurotoxic effect of iodide and its mechanism, a human dopaminergic neuroblastoma cell line (SH-SY5Y) was treated with different concentrations of potassium iodide (KI). The results showed that excessive iodide could decrease cell viability, reduce glutathione (GSH) and superoxide dismutase (SOD), and increase the degree of autophagy (by changing the cellular ultrastructure and raising the autophagy-related mRNA and protein expression of LC3, Beclin1, and p62), which were correlated with the immunofluorescence labeling. Furthermore, treatment with the autophagy inhibitor 3-methyladenine (3MA), antioxidant N-acetylcysteine (NAC) and 30 mM KI for 24 h was conducted in the following research. 3MA significantly decreased autophagy-related mRNA and protein expression and improved cell viability, indicating that excess iodide induced autophagic cell death. In addition, oxidative stress regulated autophagy, reflected by the results that NAC decreased the mRNA and protein expression of LC3, Beclin1, and p62. In summary, autophagic cell death mediated by oxidative stress may participate in excessive iodide-induced SH-SY5Y cell death.

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“…For E. perfoliatum ethanolic extract, IC 50 values between 12 and 14 μg/ml were obtained after 24 h exposure in three distinct mammalian cell lines [32]. In MCF7 breast cancer cells a time dependent effect was also observed for E. odoratum ethyl acetate extract (IC 50 of 65.72, 83.88 μg/ml and 92.84 μg/ml for 24, 48 and 72 h, respectively) while for acetone extract higher IC 50 values were obtained but without a direct correlation with exposure time (133.9, 163.0 and 147.8 μg/ml for 24, 48, and 72 h respectively) [33]. The immediate cytotoxicity observed here for EcEE is lower than that obtained for E. perfoliatum ethanolic extract and higher than that of ethyl acetate or acetone extracts from E. odoratum .…”

Section: Discussionmentioning

confidence: 99%

Cytotoxicity of Eupatorium cannabinum L. ethanolic extract against colon cancer cells and interactions with Bisphenol A and Doxorubicin

Ribeiro

Ressurreição

Viegas

et al. 2014

BMC Complement Altern Med

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BackgroundEupatorium cannabinum L. has long been utilized in traditional medicine, however no information is available regarding cellular effects of full extracts. Here we assessed the effects of E. cannabinum ethanolic extract (EcEE) on the colon cancer line HT29. Potential interactions with bisphenol A (BPA) a synthetic phenolic compound to which humans are generally exposed and a commonly used chemotherapeutic agent, doxorubicin (DOX) were also evaluated.MethodsHT29 cells were exposed to different concentrations (0.5 to 50 μg/ml) of EcEE alone or in combination with BPA or DOX. Cell viability was analyzed through resazurin assay. Gene transcription levels for NCL, FOS, p21, AURKA and bcl-xl were determined through qRT-PCR. Cytological analysis included evaluation of nuclear and mitotic anomalies after DAPI staining, immunodetection of histone H3 lysine 9 acetylation (H3K9ac) and assessment of DNA damage by TUNEL assay.ResultsSevere loss of HT29 cell viability was detected for 50 μg/ml EcEE immediately after 24 h exposure whereas the lower concentrations assayed (0.5, 5 and 25 μg/ml) resulted in significant viability decreases after 96 h. Exposure to 25 μg/ml EcEE for 48 h resulted in irreversible cell damage leading to a drastic decrease in cell viability after 72 h recovery in EcEE-free medium. 48 h 25 μg/ml EcEE treatment also induced alteration of colony morphology, H3K9 hyperacetylation, transcriptional up regulation of p21 and down regulation of NCL, FOS and AURKA, indicating reduced proliferation capacity. This treatment also resulted in drastic mitotic and nuclear disruption accompanied by up-regulation of bcl-xl, limited TUNEL labeling and nuclear size increase, suggestive of a non-apoptocic cell death pathway. EcEE/BPA co-exposure increased mitotic anomalies particularly for the lowest EcEE concentration, although without major effects on viability. Conversely, EcEE/DOX co-exposure decreased cell viability in relation to DOX for all EcEE concentrations, without affecting the DOX-induced cell cycle arrest.ConclusionsEcEE has cytotoxic activity on HT29 cancer cells leading to mitotic disruption and non-apoptotic cell death without severe induction of DNA damage. Interaction experiments showed that EcEE can increase BPA aneugenic effects and EcEE synergistic effects with DOX supporting a potential use as adjuvant in chemotherapeutic approaches.

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Autophagic Cell Death Is Induced by Acetone and Ethyl Acetate Extracts fromEupatorium odoratum In Vitro: Effects on MCF-7 and Vero Cell Lines

Cited by 21 publications

References 28 publications

Cytotoxic effects of Euterpe oleracea Mart. in malignant cell lines

Cytotoxic effects of Euterpe oleracea Mart. in malignant cell lines

Oxidative stress‐mediated autophagic cell death participates in the neurotoxic effect on SH‐SY5Y cells induced by excessive iodide

Cytotoxicity of Eupatorium cannabinum L. ethanolic extract against colon cancer cells and interactions with Bisphenol A and Doxorubicin

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