Curcumin Induces Apoptosis in SGC-7901 Gastric Adenocarcinoma Cells via Regulation of Mitochondrial Signaling Pathways

Xue, Xindong; Yu, Jinlong; Sun, Deqing; Kong, Feng-Ming; Qu, Xian‐Jun; Zou, Wen; Wu, Jing; Wang, Rong-Mei

doi:10.7314/apjcp.2014.15.9.3987

Cited by 47 publications

(33 citation statements)

References 35 publications

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“…The mitochondria-mediated apoptotic pathway is characterized by loss of MMP and release of cytochrome c from mitochondria into the cytoplasm (28). In the present study, the mitochondrial-specific cationic dye, JC-1, was used to confirm the loss of MMP upon exposure to curcumin, and an immunofluorescence assay showed cytochrome c translocation, occurring in a dose-dependent manner.…”

Section: Discussionmentioning

confidence: 82%

Curcumin induces the apoptosis of A549 cells via oxidative stress and MAPK signaling pathways

Yao

Lin

Wang

et al. 2015

International Journal of Molecular Medicine

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Abstract. Curcumin has been found to exhibit anticancer activity and certain studies have shown that curcumin triggers the apoptosis of human A549 lung adenocarcinoma cells. However, the mechanism underlying curcumin-mediated apoptosis is not completely understood. The present study was designed to investigate the effect of curcumin on the induction of apoptosis and apoptosis-related factors in human A549 lung adenocarcinoma cells. Treatment of A549 cells with curcumin caused a concentration-dependent inhibition of cell growth and an increase in apoptosis, as confirmed by THE MTT assay, flow cytometry and morphology analysis. Curcumin-treatment of A549 cells induced a loss of the mitochondrial membrane potential and increased cytosolic cytochrome c. Furthermore, curcumin-induced apoptosis was accompanied by changes in intracellular oxidative stress-related enzymes, including decreased intracellular reactive oxygen species levels, increased superoxide dismutase and decreased malondialdehyde and 4-hydroxynonenal. In addition, induction of apoptosis was also accompanied by phosphorylation and activation of mitogen-activated protein kinase signaling pathway factors c-Jun N-terminal kinase, p38 and extracellular signal-regulated kinase. IntroductionLung cancer is the main leading cause of cancer-related fatality worldwide, with a rapidly increasing rate in China and other Asian countries (1-4). Chemotherapy is currently the most frequently used treatment for lung cancer and other types of cancer. However, while this method of treatment kills cancer cells, it also destroys some normal cells. Thus, the identification of novel natural compounds with low toxicity and high selectivity for killing cancer cells is a significant area in cancer research (5), and several natural products have been used as alternative treatments for cancer (6,7).Curcumin, a natural and crystalline compound isolated from the plant Curcuma longa, has been widely studied for its anti-inflammatory, antiangiogenic, antioxidant and anticancer effects in Chinese systems of medicine (8,9). Additionally, previous studies have shown that curcumin exhibits antiproliferative and anticarcinogenic properties in a wide variety of cell lines and animals (10,11). Previous studies have demonstrated that curcumin inhibits the growth and apoptosis of human A549 lung adenocarcinoma cells (12)(13)(14). However, the mechanisms of curcumin-induced apoptosis via oxidative stress remain unclear.The physiological status of the reactive oxygen species (ROS) levels can regulate cell proliferation: When intracellular ROS levels are above a certain threshold, ROS inhibit the cell cycle, leading to increased cell apoptosis and necrosis. In the tumor cells it often maintains a higher state of oxidation, with higher levels of oxygen free radicals and lower levels of the antioxidant enzyme activity. This higher oxidation state can activate certain transcription factors and associated genes, such as NF-κB and API, thus, ensuring the survival, proliferation and migration of tumor ...

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Section: Discussionmentioning

confidence: 82%

Curcumin induces the apoptosis of A549 cells via oxidative stress and MAPK signaling pathways

Yao

Lin

Wang

et al. 2015

International Journal of Molecular Medicine

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“…Apoptosis can be triggered by various stimuli, including death receptor-mediated signaling and intracellular stress (Banjerdpongchai and Kongtawelert, 2011). It is well known that Cyt C triggers the activation of caspase cascade in the intrinsic apoptotic pathway if released from mitochondrial membrane gap into cytoplasm (Garrido et al, 2006;Xue et al, 2014). Cyt C is so called the Achilles' heel in apoptosis, for its promotion in the process of apoptosis irreversibly (Kulikov et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

Bufalin Induces Mitochondrial Pathway-Mediated Apoptosis in Lung Adenocarcinoma Cells

Ding

Zhang²,

Huang³

et al. 2015

Asian Pacific Journal of Cancer Prevention

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Background: To evaluate the effects of bufalin in A549 human lung adenocarcinoma epithelial cells in vitro and assess the underlying mechanisms. Materials and Methods: Human A549 non-small cell lung cancer (NSCLC) cells were treated with various concentrations of bufalin. Cell proliferation was measured by CCK-8 assay, apoptotic cell percentage was calculated by flow cytometry and morphological change was observed by inverted phase contrast microscopy/transmission electron microscopy. In addition, the membrane potential of mitochondria was detected by JC-1 fluorescence microscopy assay, and the related protein expression of cytochrome C and caspase-3 was analyzed by Western blotting. Results: Bufalin could inhibit the proliferation of A549 cells via induction of apoptosis, with the evidence of characteristic morphological changes in the nucleus and mitochondria. Furthermore, bufalin decreased the mitochondrial membrane potential with up-regulation of cytochrome C in the cytosol, and activation of caspase-3. Conclusions: Bufalin inhibits the proliferation of A549 cells and triggers mitochondria-dependent apoptosis, pointing to therapeutic application for NSCLC.

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“…Flow cytometry showed that the cells treated with AHL have effectively arrested in G2/M phase. Abnormality in cell cycle regulation implies the following apoptosis event, which leads to the proliferation inhibition of HepG-2 cells (Xue et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Alkaloids from Beach Spider Lily (Hymenocallis littoralis) Induce Apoptosis of HepG-2 Cells by the Fas-signaling Pathway

Yu-bin

Chen²,

Zhu³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Alkaloids are the most extensively featured compounds of natural anti-tumor herbs, which have attracted much attention in pharmaceutical research. In our previous studies, a mixture of major three alkaloid components (5, 6-dihydrobicolorine, 7-deoxy-trans-dihydronarciclasine, littoraline) from Hymenocallis littoralis were extracted, analyzed and designated as AHL. In this paper, AHL extracts were added to human liver hepatocellular cells HepG-2, human gastric cancer cell SGC-7901, human breast adenocarcinoma cell MCF-7 and human umbilical vein endothelial cell EVC-304, to screen one or more AHL-sensitive tumor cell. Among these cells, HepG-2 was the most sensitive to AHL treatment, a very low dose (0.8μg/ml) significantly inhibiting proliferation . The nontumor cell EVC-304, however, was not apparently affected. Effect of AHL on HepG-2 cells was then explored. We found that the AHL could cause HepG-2 cycle arrest at G2/M checkpoint, induce apoptosis, and interrupt polymerization of microtubules. In addition, expression of two cell cycle-regulated proteins, CyclinB1 and CDK1, was up-regulated upon AHL treatment. Up-regulation of the Fas, Fas ligand, Caspase-8 and Caspase-3 was observed as well, which might imply roles for the Fas/FsaL signaling pathway in the AHL-induced apoptosis of HepG-2 cells.

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Curcumin Induces Apoptosis in SGC-7901 Gastric Adenocarcinoma Cells via Regulation of Mitochondrial Signaling Pathways

Cited by 47 publications

References 35 publications

Curcumin induces the apoptosis of A549 cells via oxidative stress and MAPK signaling pathways

Curcumin induces the apoptosis of A549 cells via oxidative stress and MAPK signaling pathways

Bufalin Induces Mitochondrial Pathway-Mediated Apoptosis in Lung Adenocarcinoma Cells

Alkaloids from Beach Spider Lily (Hymenocallis littoralis) Induce Apoptosis of HepG-2 Cells by the Fas-signaling Pathway

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