Aloe emodin inhibits colon cancer cell migration/angiogenesis by downregulating MMP-2/9, RhoB and VEGF via reduced DNA binding activity of NF-κB

Suboj, Priya; Babykutty, Suboj; Gopi, Deepak Roshan Valiyaparambil; Naveed, Ammara; Srinivas, Priya; Gopala, Srinivas

doi:10.1016/j.ejps.2011.12.012

Cited by 118 publications

(61 citation statements)

References 47 publications

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“…Emodin exerts its pleiotropic anti-cancer effects through diverse mechanisms including the activation of caspase-3 [23] and upregulation of p53 and p21 [26]. Moreover, emodin has been reported to inhibit the kinase activity/activation of p56lck, HER2/neu [21], casein kinase [27], NF-jB [28], activator protein 1 [29,30], AKT [30], matrix metalloproteinases [29,31], and the expression of chemokine receptor CXCR4 [32]. Our findings specifically in HCC cells clearly indicate that this quinone can enhance TRAIL-induced apoptosis through the downregulation of antiapoptotic proteins, upregulation of death receptors and the activation of C/EBP homologous protein (CHOP).…”

Section: Introductionmentioning

confidence: 99%

An anthraquinone derivative, emodin sensitizes hepatocellular carcinoma cells to TRAIL induced apoptosis through the induction of death receptors and downregulation of cell survival proteins

et al. 2013

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Recombinant tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is currently under clinical trials for cancer, however many tumor cells, including hepatocellular carcinoma (HCC) develop resistance to TRAIL-induced apoptosis. Hence, novel agents that can alleviate TRAIL-induced resistance are urgently needed. In the present report, we investigated the potential of emodin to enhance apoptosis induced by TRAIL in HCC cells. As observed by MTT cytotoxicity assay and the externalization of the membrane phospholipid phosphatidylserine, we found that emodin can significantly potentiate TRAIL-induced apoptosis in HCC cells. When investigated for the mechanism(s), we observed that emodin can downregulate the expression of various cell survival proteins, and induce the cell surface expression of both TRAIL receptors, death receptors (DR) 4 as well as 5. In addition, emodin increased the expression of C/EBP homologous protein (CHOP) in a time-dependent manner. Knockdown of CHOP by siRNA decreased the induction of emodin-induced DR5 expression and apoptosis. Emodin-induced induction of DR5 was mediated through the generation of reactive oxygen species (ROS), as N-acetylcysteine blocked the induction of DR5 and the induction of apoptosis. Also, the knockdown of X-linked inhibitor of apoptosis protein by siRNA significantly reduced the sensitization effect of emodin on TRAILinduced apoptosis. Overall, our experimental results clearly indicate that emodin can indeed potentiate TRAIL-induced Aruljothi Subramaniam and Ser Yue Loo contributed equally to this work.

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Section: Introductionmentioning

confidence: 99%

An anthraquinone derivative, emodin sensitizes hepatocellular carcinoma cells to TRAIL induced apoptosis through the induction of death receptors and downregulation of cell survival proteins

et al. 2013

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“…AE can influence all key steps involved in the angiogenesis, including the local proliferation of endothelial cells, migration, invasion and finally differentiation and new vessels formation. Data showed that AE inhibits cell proliferation and in vitro cell migration/invasion and tube formation of human umbilical vein endothelial cells (HUVECs) [11]. The ability of AE treatment to inhibit the proliferation of primary bovine aortic endothelial cells (BAEC) have been also proven [10].…”

Section: Introductionmentioning

confidence: 99%

“…Hundreds of natural compounds of plant and animal origin have properties of angiogenic inhibitors [6-. One of them is aloe-emodin [1,8-dihydroxy-3-hydroxymethylanthraquinone], bioactive hydroxyanthraquinone Aloe barbadensis Miller (Aloe vera), Rheum officinale, as well as in leaves and roots of other plants [9], showing in vitro and antitumor activity and anti-angiogenic properties [10,11].…”

Section: Introductionmentioning

confidence: 99%

Aloe-emodin triggers ROS and Ca 2+ production and decreases the levels of mitochondrial membrane potential of human brain capillary endothelial cells

Dimova¹,

Danova²,

Nikolova³

et al. 2017

ijpm

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A b s t r a c tThe aim of this hydroxyanthraquinone aloe hCMEC/D3 and to assess the cellular response in the early stage of treatment in order to extend the k capillary endothelial cells hCMEC/D3 were treated with a μM) for a period of 24 hours. The cell viability was determined by MTS assay. The cellul adenosine triphosphate (ATP) levels were evaluated by CellTiter intracellular reactive oxygen species (ROS) were determined by 2',7' H2DCFDA) fluorescence assay. The mitochondrial membrane potential (M using tetramethylrhodamine methyl ester (TMRM) staining, while Fluo the intracellular free Ca using the Arrays Twenty µM, decreased the cell viability as well as the intracellular ATP levels in a dose manner. Increased ROS production and disruption of the have a increased intracellular calcium levels. Our results collectively indicate that AE inhibits proliferation of human brain micro cells via a mechanism involving ROS mitochondrial damage.

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“…(88) Aloe emodin, an anthraquinone from Rheum palmatum L., has anti-migratory and anti-angiogenic activities in colon cancer cells by down-regulating expression of MMP-2/9, RhoB and VEGF. (89) Honokiol, a major phenolic compound isolated from the root and stem bark of magnolia, inhibited the expression of MMP-9 in PANC-1 cells in vitro and VEGF in tumor tissue in vivo in an athymic mouse tumor model. (90) Immune Suppression…”

Section: Angiogenesis and Lymphangiogenesismentioning

confidence: 99%

Targeting tumor-associated macrophages by anti-tumor Chinese materia medica

Sun

Gao

et al. 2017

Chin. J. Integr. Med.

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Infiltration of the tumor microenvironment (TME) by immune and inflammatory cells is involved in promoting tumorigenesis, tumor progression, local invasion and metastasis.(1) Tumor-associated macrophages (TAMs), a prominent and abundant inflammatory component of solid and hematological malignancies, express a pro-and anti-tumor effect in all stages of carcinogenesis. Asian region. According to the theory of Chinese medicine (CM) and its practice, some Asian region. According to the theory of Chinese medicine (CM) and its practice, some prescriptions of CM regulate the body's internal environment possibly including the prescriptions of CM regulate the body's internal environment possibly including the remodeling the tumor microenvironment (TME). Here we brie y summarize the pivotal remodeling the tumor microenvironment (TME). Here we brie y summarize the pivotal effects of TAMs in shaping the TME and promoting tumorigenesis, invasion, metastasis effects of TAMs in shaping the TME and promoting tumorigenesis, invasion, metastasis and immunosuppression. Furthermore, we illustrate the effects and mechanisms of CMM targeting TAMs in antiand immunosuppression. Furthermore, we illustrate the effects and mechanisms of CMM targeting TAMs in antitumor therapy. Finally, we reveal the CMM's dual-regulatory and multi-targeting functions on regulating TAMs, tumor therapy. Finally, we reveal the CMM's dual-regulatory and multi-targeting functions on regulating TAMs, and hopefully, provide the theoretical basis for CMM clinical practice related to cancer therapy. and hopefully, provide the theoretical basis for CMM clinical practice related to cancer therapy.

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Aloe emodin inhibits colon cancer cell migration/angiogenesis by downregulating MMP-2/9, RhoB and VEGF via reduced DNA binding activity of NF-κB

Cited by 118 publications

References 47 publications

An anthraquinone derivative, emodin sensitizes hepatocellular carcinoma cells to TRAIL induced apoptosis through the induction of death receptors and downregulation of cell survival proteins

An anthraquinone derivative, emodin sensitizes hepatocellular carcinoma cells to TRAIL induced apoptosis through the induction of death receptors and downregulation of cell survival proteins

Aloe-emodin triggers ROS and Ca 2+ production and decreases the levels of mitochondrial membrane potential of human brain capillary endothelial cells

Targeting tumor-associated macrophages by anti-tumor Chinese materia medica

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