Curcumin-induced Histone Hypoacetylation Enhances Caspase-3-dependent Glioma Cell Death and Neurogenesis of Neural Progenitor Cells

Kang, Soo‐Kyung; Cha, Seung-Heun; Jeon, Hyo-Gon

doi:10.1089/scd.2006.15.165

Cited by 159 publications

(96 citation statements)

References 29 publications

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“…In the present study, curcumin affected intracellular oxidative stress, decreased ROS and increased SOD activity, further reducing the generation of MDA and 4-HNE (32). These changes trigger the intrinsic apoptotic pathway: HSP70 expression is restrained, the proapoptotic protein Bax and antiapoptotic protein Bcl-2 are activated, MMP is lost, cytochrome c is released into the cytoplasm, the caspase-9/3 classical apoptotic pathway is activated, and eventually cells die (33,34). When cells were pretreated with the HSP70 inhibitor, the indicators of the redox state did not show any change, however, MMP, cytochrome c and the Bax/Bcl-2 ratio were significantly changed, and cells were prevented from undergoing cell apoptosis.…”

Section: Discussionmentioning

confidence: 51%

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: 51%

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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“…Accordingly, caspase-3 activation was increased by DNC. Previous studies reported that the induction of caspase-3 by curcumin in glioma cells may involve histone hypoacetylation 43 and activation of the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL/Apo2L) pathway. 44 Formerly, the role of DNC in apoptosis induction was reported in A431 cells -a cell line model of epidermoid carcinoma -in a PARP (poly [adenosine diphosphate ribose] polymerase-dependent) pathway, indicating that DNC induces cancer cell death via triggering of the apoptosis pathways.…”

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confidence: 99%

Dendrosomal curcumin nanoformulation downregulates pluripotency genes via miR-145 activation in U87MG glioblastoma cells

Mirgani¹,

Isacchi²,

Sadeghizadeh³

et al. 2014

IJN

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Glioblastoma is an invasive tumor of the central nervous system. Tumor recurrence resulting from ineffective current treatments, mainly due to the blood–brain barrier, highlights the need for innovative therapeutic alternatives. The recent availability of nanotechnology represents a novel targeted strategy in cancer therapy. Natural products have received considerable attention for cancer therapy because of general lower side effects. Curcumin is a new candidate for anticancer treatment, but its low bioavailability and water solubility represent the main disadvantages of its use. Here, curcumin was efficiently encapsulated in a nontoxic nanocarrier, termed dendrosome, to overcome these problems. Dendrosomal curcumin was prepared as 142 nm spherical structures with constant physical and chemical stability. The inhibitory role of dendrosomal curcumin on the proliferation of U87MG cells, a cellular model of glioblastoma, was evaluated by considering master genes of pluripotency and regulatory miRNA (microribonucleic acid). Methylthiazol tetrazolium assay and flow cytometry were used to detect the antiproliferative effects of dendrosomal curcumin. Annexin-V-FLUOS and caspase assay were used to quantify apoptosis. Real-time polymerase chain reaction was used to analyze the expression of OCT4 (octamer binding protein 4) gene variants ( OCT4A , OCT4B , and OCT4B1 ), SOX-2 (SRY [sex determining region Y]-box 2) , Nanog , and miR-145 . Dendrosomal curcumin efficiently suppresses U87MG cells growth with no cytotoxicity related to dendrosome. Additionally, the accumulation of cells in the SubG 1 phase was observed in a time- and dose-dependent manner as well as higher rates of apoptosis after dendrosomal curcumin treatment. Conversely, nonneoplastic cells were not affected by this formulation. Dendrosomal curcumin significantly decreased the relative expression of OCT4A , OCT4B1 , SOX-2 , and Nanog along with noticeable overexpression of miR-145 as the upstream regulator. This suggests that dendrosomal curcumin reduces the proliferation of U87MG cells through the downregulation of OCT4 (octamer binding protein 4) variants and SOX-2 (SRY [sex determining region Y]-box 2) in an miR-145 -dependent manner.

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“…Additionally, curcumin suppresses the p300/CBP HAT activity dependent chromatin transcription (Morimoto et al 2008). The findings of Kang et al (2006) illustrated that curcumin activated the poly(adenosine diphosphate ribose) polymerase and caspase-3 mediated apoptosis by inducing histone hypoacetylation in brain glioma cell lines. Likewise, curcumin lowers acetylation of RelA by suppressing p300 that attenuates interaction with IjBa.…”

Section: Epigenetic Role Of Curcumin -Histone Deacetylases and Acetylmentioning

confidence: 98%

Curcumin and its allied analogues: epigenetic and health perspectives - a review

Imran¹,

Nadeem²,

Khan³

et al. 2017

Czech J. Food Sci.

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Curcumin (diferuoyl methane) is a yellow active ingredient present in turmeric. It is a homodimer of feruloylmethane that comprises a hydroxyl and methoxy group (heptadiene with two Michael acceptors), and α-, β-diketone. It contains various metabolites, i.e. hexahydrocurcumin (HHC), tetrahydrocurcumin (THC), octahydrocurcumin (OHC), dihydrocurcumin (DHC), curcumin sulphate, and curcumin glucuronide. Curcumin has been proven the most effective histone deacetylase (HDAC) inhibitor in HeLa nuclear extracts. It has the ability to affect the Akt, growth factors, NF-kB, and metastatic and angiogenic pathways. Curcumin has a strong therapeutic or preventive potential against several major human ailments, i.e. suppression of inflammation, cardiovascular, diabetes, tumorigenesis, chronic fatigue, antidepressant and neurological activities, depression, loss of muscle and bone, and neuropathic pain. In future, higher utilisation of curcumin as an active agent in food based products is required to curtail the human health disorders.

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Curcumin-induced Histone Hypoacetylation Enhances Caspase-3-dependent Glioma Cell Death and Neurogenesis of Neural Progenitor Cells

Cited by 159 publications

References 29 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

Dendrosomal curcumin nanoformulation downregulates pluripotency genes via miR-145 activation in U87MG glioblastoma cells

Curcumin and its allied analogues: epigenetic and health perspectives - a review

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