Protein kinase C involvement in aloe‐emodin‐ and emodin‐induced apoptosis in lung carcinoma cell

Lee, Hong‐Zin

doi:10.1038/sj.bjp.0704342

Cited by 108 publications

(76 citation statements)

References 37 publications

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“…In addition, it was observed that aloe-emodin-induced apoptosis in human hepatocellular carcinoma cell lines HepG2 and Hep3B was accompanied by the induction of p53 and p21 expression (5). Another report suggests that the decrease in the expression of protein kinase Cδ and ε isoforms plays a critical role in aloe-emodin-induced apoptosis (21). A similar role of protein kinase C was observed in U-937 glioma cells (6).…”

Section: Discussionmentioning

confidence: 53%

“…It was reported that, using the human lung squamous carcinoma cell line CH27, apoptosis induced by aloe-emodin was associated with changes in the expression of members of the Bcl-2 family apoptosis regulators (i.e., increase in the Bax level and decrease in Bcl-XL). Aloe-emodin was found to cause cytochrome c release from mitochondria (21). In addition, it was observed that aloe-emodin-induced apoptosis in human hepatocellular carcinoma cell lines HepG2 and Hep3B was accompanied by the induction of p53 and p21 expression (5).…”

Section: Discussionmentioning

confidence: 88%

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Aloe-emodin, an anthraquinone, in vitro inhibits proliferation and induces apoptosis in human colon carcinoma cells

Lin

Uen²

2010

Oncology Letters

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Abstract. The present study aimed to investigate the anticancer effect of aloe-emodin, an anthraquinone compound present in the leaves of Aloe vera, on two human colon carcinoma cell lines, DLD-1 and WiDr. Colon carcinoma cells were treated with various concentrations of aloe-emodin for different durations. Cell viability was measured by sodium 3'-[1-(phenylamino-carbonyl)-3,4-tetrazolium]-bis(4-methoxy-6-nitro)benzene-sulfonic acid hydrate assay. DNA fragmentation was analyzed by agarose gel electrophoresis. Nuclear shrinkage was visualized by Hoechst 33258 staining. Western blotting was used to indicate the release of apoptosisinducing factor and cytochrome c from mitochondria and the phosphorylation of Bid. Caspase-3 and casein kinase II activities were measured by the respective assays. Cell viability analyses showed that aloe-emodin induced cell death in a dose-and time-dependent manner. Notably, the WiDr cells were more sensitive to aloe-emodin than the DLD-1 cells. Aloe-emodin caused the release of apoptosis-inducing factor and cytochrome c from mitochondria, followed by activation of caspase-3 leading to DNA fragmentation, nuclear shrinkage and apoptosis. In addition, exposure of colon carcinoma cells to aloe-emodin suppressed the casein kinase II activity in a time-dependent manner and was accompanied by a reduced phosphorylation of Bid, a downstream substrate of casein kinase II and a pro-apoptotic molecule. These findings showed that the inhibition of casein kinase II activity, the release of apoptosis-inducing factor and cytochrome c, and the caspase-3 activation are involved in aloe-emodin-mediated apoptosis in colon carcinoma cells.

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Section: Discussionmentioning

confidence: 53%

Section: Discussionmentioning

confidence: 88%

Aloe-emodin, an anthraquinone, in vitro inhibits proliferation and induces apoptosis in human colon carcinoma cells

Lin

Uen²

2010

Oncology Letters

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“…However, several studies indicated that emodin-induced apoptosis was mediated by ROS-generated (Jing et al, 2002;Su et al, 2005) and caspase-and mitochondrial-dependent pathways in human cervical cancer cells (Srinivas et al, 2003). Emodin induced apoptosis in human lung squamous cell carcinoma (Zhang et al, 1999;Lee, 2001), and HepG2/C3A cells were mediated through the activation of p53, p21, Fas/APO-1, and caspase-3 (Shieh et al, 2004). Emodin down-regulates androgen receptor and inhibits prostate cancer cell growth (Cha et al, 2005), and the oxidative injury in lung cancer A549 cells mediated by emodin acts as an early and upstream change in the cell death cascade to antagonize cytoprotective ERK and AKT signaling.…”

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confidence: 99%

Emodin Has Cytotoxic and Protective Effects in Rat C6 Glioma Cells: Roles of Mdr1a and Nuclear Factor κB in Cell Survival

Kuo¹,

Yang²,

Meng³

et al. 2009

J Pharmacol Exp Ther

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ABSTRACT1,3,8-Trihydroxy-6-methylanthaquinone (emodin) is recognized as an antiproliferative compound. In the present study, however, we show that emodin has both toxic and survival effects in glioma cells and that the survival effects involve Mdr1a. Emodin inhibited the proliferation and induced apoptosis of C6 cells in a 12-h treatment, but C6 cells survived a 72-h drug treatment, indicating resistance to emodin. Emodin-induced apoptosis was reduced by inhibition of the expression and activation of apoptosis-associated proteins including p53, Bax, Bcl-2, Fas, and caspase-3. C6 cells could express antioxidant proteins (superoxide dismutase and catalase) to decrease reactive oxygen species-induced cytotoxicity of emodin and overexpress multidrug resistance genes (Mdr1a, MRP2, MRP3, and MRP6) to decrease the intracellular accumulation of emodin. Electrophoretic mobility shift analysis showed that emodin decreased nuclear factor B (NF-B) expression in 24 h of treatment, but in 48 h, emodin increased NF-B activity. A confocal microscope showed that emodin induced NF-B translocation from cytoplasm to nuclei. C6 cells would activate the mitogen-activated protein kinase survival pathway and express the DNA repair gene (MGMT) and associated proteins (PARP and XRCC1) to recover the cell activity. C6 cells also expressed GRP78 to decrease emodin-induced endoplasmic reticulum (ER) stress that would cause apoptosis in C6 cells, and GRP78 inhibited the expression of GADD153 to enhance the expression of Bcl-2 that could balance the ER-and mitochondria-induced apoptosis of C6 cells.

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“…[7][8] Although emodin has a high degree of inhibitory activity against various types of tumor cells, the mechanisms of action differ from each other. Some scholars believe that emodin has an apoptosis inducing effect on a variety of tumor cells; its signal transduction pathways for induction of apoptosis mainly include Bax.…”

Section: Discussionmentioning

confidence: 99%

Inhibitory effect of emodin on human hepatoma cell line SMMC-7721 and its mechanism

Zhang¹,

Chen²,

Zhang³

et al. 2015

Afr H. Sci.

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Background: Da Huang (Radix et Rhizoma Rhei) is the dried root or rhizome of Rheum palmatum L., Rheum tanguticum Maxim ex Balf. or Rheum officinale Braill of family Polygonaceae. It has heat clearing, damp drying, fire purging and toxin removing effects. Because of its definite curative efficacy, it has been widely applied in clinical settings. Objective: To study the inhibitory effect of emodin on human hepatoma cell line SMMC-7721 and its mechanism. Methods: MTT assay, flow cytometry and electron microscopy were used to investigate the inhibitory effect of different concentrations of emodin on human hepatoma cell line SMMC-7721.

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Protein kinase C involvement in aloe‐emodin‐ and emodin‐induced apoptosis in lung carcinoma cell

Cited by 108 publications

References 37 publications

Aloe-emodin, an anthraquinone, in vitro inhibits proliferation and induces apoptosis in human colon carcinoma cells

Aloe-emodin, an anthraquinone, in vitro inhibits proliferation and induces apoptosis in human colon carcinoma cells

Emodin Has Cytotoxic and Protective Effects in Rat C6 Glioma Cells: Roles of Mdr1a and Nuclear Factor κB in Cell Survival

Inhibitory effect of emodin on human hepatoma cell line SMMC-7721 and its mechanism

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