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

Kello, Martin; Takáč, Peter; Kubatka, Peter; Kuruc, Tomáš; Petrova, Klaudia; Mojžiš, Ján

doi:10.3390/biom10010139

Cited by 34 publications

(23 citation statements)

References 56 publications

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“…[ 54 ] We further determined cell demise and apoptotic cell decease happened in TE‐13 cells in a time‐dependent manner by clove oil, which holds eugenol with 80% cell death while DU‐145 cells displayed negligible cell death. [ 55 ] The same results were observed in propidium iodide staining also in which Eu‐Pi/PHB‐PEG‐NC (5–7.5 μM) demonstrates red fluorescence of apoptotic cells, which is displayed in Figure 8. The control displays a normal appearance without any red fluorescence.…”

Section: Resultssupporting

confidence: 72%

“…[54] We further determined cell demise and DU-145 cells displayed negligible cell death. [55] The same results were observed in propidium iodide staining also in which Eu-Pi/PHB-PEG-NC…”

Section: Eu-pi/phb-peg-nc Increases Intracellular Ros In C666-1 Cellssupporting

confidence: 68%

“…The preceding microscopic study evaluated the accuracy of trypan blue in differentiating viable and nonviable cells that showed interruption of cellular organelles, while viable cells show membrane integrity. [ 55 ]…”

Section: Resultsmentioning

confidence: 99%

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Eugenol–piperine loaded polyhydroxy butyrate/polyethylene glycol nanocomposite‐induced apoptosis and cell death in nasopharyngeal cancer (C666‐1) cells through the inhibition of the PI3K/AKT/mTOR signaling pathway

Sun

Veeraraghavan

Surapaneni³

et al. 2021

J Biochem & Molecular Tox

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Nasopharyngeal cancer is a malignancy developing from the nasopharynx epithelium due to smoking and nitrosamine‐containing foods. Nasopharyngeal cancer is highly endemic to Southeast Asia. Eugenol and piperine have shown many anticancer activities on numerous cancer types, like colon, lung, liver, and breast cancer. In this study, we amalgamated eugenol and piperine loaded with a polyhydroxy butyrate/polyethylene glycol nanocomposite (Eu‐Pi/PHB‐PEG‐NC) for better anticancer results against nasopharyngeal cancer (C666‐1) cells. In the current study, nasopharyngeal cancer cell lines C666‐1 were utilized to appraise the cytotoxic potential of Eug‐Pip‐PEG‐NC on cell propagation, programmed cell death, and relocation. Eu‐Pi/PHB‐PEG‐NC inhibits cellular proliferation on C666‐1 cells in a dose‐dependent manner, and when compared with 20 µg/ml, 15 µg/ml of loaded mixture evidently restrained the passage aptitude of C666‐1 cells, this was attended with a downregulated expression of mitochondrial membrane potential. Treatment with 15 µg/ml Eu‐Pi/PHB‐PEG‐NC suggestively amplified cell apoptosis in the C666‐1 cells. Furthermore, its cleaved caspase‐3, 8, and 9 and Bax gene expression was augmented and Bcl‐2 gene expression was diminished after Eu‐Pi/PHB‐PEG‐NC treatment. Additionally, our data established that the collective effect of Eu‐Pi/PHB‐PEG‐NC loaded micelles inhibited the expansion of C666‐1 cells augmented apoptosis connected with the intrusion of PI3K/Akt/mTOR signaling pathway.

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Section: Resultssupporting

confidence: 72%

“…[54] We further determined cell demise and DU-145 cells displayed negligible cell death. [55] The same results were observed in propidium iodide staining also in which Eu-Pi/PHB-PEG-NC…”

Section: Eu-pi/phb-peg-nc Increases Intracellular Ros In C666-1 Cellssupporting

confidence: 68%

See 1 more Smart Citation

Eugenol–piperine loaded polyhydroxy butyrate/polyethylene glycol nanocomposite‐induced apoptosis and cell death in nasopharyngeal cancer (C666‐1) cells through the inhibition of the PI3K/AKT/mTOR signaling pathway

Sun

Veeraraghavan

Surapaneni³

et al. 2021

J Biochem & Molecular Tox

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show abstract

“…Pro-apoptotic activity of ERK has been reported previously. Aberrant ERK activation by neurotoxic Aβ 42 peptide leads to apoptosis in neurons [ 63 ], and prolonged activation of ERK beyond 24 and 48 h was associated with apoptosis induced by clove bud extracts in MCF-7 cells [ 64 ]. There are also reports showing that ERK activation by oxidative stress is associated with apoptosis in renal [ 65 ] and fibroblast cell lines [ 66 ].…”

Section: Discussionmentioning

confidence: 99%

Loss of Caveolin-1 Is Associated with a Decrease in Beta Cell Death in Mice on a High Fat Diet

Urzúa

Murillo

Castro-Sepúlveda

et al. 2020

IJMS

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Elevated free fatty acids (FFAs) impair beta cell function and reduce beta cell mass as a consequence of the lipotoxicity that occurs in type 2 diabetes (T2D). We previously reported that the membrane protein caveolin-1 (CAV1) sensitizes to palmitate-induced apoptosis in the beta pancreatic cell line MIN6. Thus, our hypothesis was that CAV1 knock-out (CAV1 KO) mice subjected to a high fat diet (HFD) should suffer less damage to beta cells than wild type (WT) mice. Here, we evaluated the in vivo response of beta cells in the pancreatic islets of 8-week-old C57Bl/6J CAV1 KO mice subjected to a control diet (CD, 14% kcal fat) or a HFD (60% kcal fat) for 12 weeks. We observed that CAV1 KO mice were resistant to weight gain when on HFD, although they had high serum cholesterol and FFA levels, impaired glucose tolerance and were insulin resistant. Some of these alterations were also observed in mice on CD. Interestingly, KO mice fed with HFD showed an adaptive response of the pancreatic beta cells and exhibited a significant decrease in beta cell apoptosis in their islets compared to WT mice. These in vivo results suggest that although the CAV1 KO mice are metabolically unhealthy, they adapt better to a HFD than WT mice. To shed light on the possible signaling pathway(s) involved, MIN6 murine beta cells expressing (MIN6 CAV) or not expressing (MIN6 Mock) CAV1 were incubated with the saturated fatty acid palmitate in the presence of mitogen-activated protein kinase inhibitors. Western blot analysis revealed that CAV1 enhanced palmitate-induced JNK, p38 and ERK phosphorylation in MIN6 CAV1 cells. Moreover, all the MAPK inhibitors partially restored MIN6 viability, but the effect was most notable with the ERK inhibitor. In conclusion, our results suggest that CAV1 KO mice adapted better to a HFD despite their altered metabolic state and that this may at least in part be due to reduced beta cell damage. Moreover, they indicate that the ability of CAV1 to increase sensitivity to FFAs may be mediated by MAPK and particularly ERK activation.

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“…Kumatakenin, a flavonoid isolated from cloves, induced apoptosis by enhancing the activity of caspase‐3, caspase‐8, and caspase‐9 in human ovarian cancer cells (SKOV3 and A2780) and in tumor‐associated macrophages (TAMs; Woo et al., 2017). Clove bud extract‐induced apoptosis, DNA damage, and oxidative stress in MCF 7 (breast cancer) cells (Kello et al., 2020).…”

Section: Studies On Cancer With Spices—major Bioactive Compoundsmentioning

confidence: 99%

Curry versus cancer: Potential of some selected culinary spices against cancer with in vitro, in vivo, and human trials evidences

et al. 2020

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Spices are dietary agents with immense potential for cancer chemo-prevention. A wide variety of spices are extensively used as food flavoring agents which possess potent antioxidant, anti-inflammatory, and anticancer properties due to the presence of certain bio-active compounds in them. In vitro, in vivo studies and clinical trials of selected spices against various types of cancer are being specified in this review. Effect of certain putative dietary spices namely turmeric, clove, garlic, ginger, fennel, black cumin, cinnamon, pepper, saffron, rosemary, and chilli along with its role in cancer are being discussed. Literature search was conducted through PubMed, Google scholar, Science direct, and Scopus using the keywords "spice," "cancer," "natural medicine," "herbal compound," "bioactive compounds." About 4,000 published articles and 127 research papers were considered to grab the brief knowledge on spices and their anticancer potential on a predefined inclusion and exclusion criteria. Practical application: Historically, spices and herbs are known for its traditional flavor, odor, and medicinal properties. Intensified risk of chronic and pervasive clinical conditions and increased cost of advanced drug treatments have developed a keen interest among researchers to explore the miscellaneous properties of herbal spices. Cancer is one of the deleterious causes of mortality affecting a huge number of populations worldwide. Arrays of cancer treatments including surgery, chemotherapy, and radiation therapy are used to compromise the disease but effective only when the size of the tumor is small. So, an effective treatment need to be developed that produces less side effects and herbal spices are found to be the promising agents. In this review, we illustrate about different in vitro, in vivo, and clinical studies of wide range of culinary spices having antineoplastic potential.

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

Cited by 34 publications

References 56 publications

Eugenol–piperine loaded polyhydroxy butyrate/polyethylene glycol nanocomposite‐induced apoptosis and cell death in nasopharyngeal cancer (C666‐1) cells through the inhibition of the PI3K/AKT/mTOR signaling pathway

Eugenol–piperine loaded polyhydroxy butyrate/polyethylene glycol nanocomposite‐induced apoptosis and cell death in nasopharyngeal cancer (C666‐1) cells through the inhibition of the PI3K/AKT/mTOR signaling pathway

Loss of Caveolin-1 Is Associated with a Decrease in Beta Cell Death in Mice on a High Fat Diet

Curry versus cancer: Potential of some selected culinary spices against cancer with in vitro, in vivo, and human trials evidences

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