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Jing Gung Chung - One of the best experts on this subject based on the ideXlab platform.

  • Aloe Emodin induces cell death through s phase arrest and caspase dependent pathways in human tongue squamous cancer scc 4 cells
    Anticancer Research, 2009
    Co-Authors: Tsan Hung Chiu, Te Chun Hsia, Jai Sing Yang, Ping Ping Wu, Chia Yu, Chin Chin Ho, Hsu Feng Lu, Gibson W Wood, Jing Gung Chung
    Abstract:

    Aloe-Emodin, one of the anthraquinones, has been shown to have anticancer activity in different kinds of human cancer cell lines. Therefore, the purpose of this study was to investigate the anti-cancer effect of Aloe-Emodin on human tongue squamous carcinoma SCC-4 cells. The results indicated that Aloe-Emodin induced cell death through S-phase arrest and apoptosis in a dose- and time-dependent manner. Treatment with 30 μM of Aloe-Emodin led to S-phase arrest through promoted p53, p21 and p27, but inhibited cyclin A, E, thymidylate synthase and Cdc25A levels. Aloe-Emodin promoted the release of apoptosis-inducing factor (AIF), endonuclease G (Endo G), pro-caspase-9 and cytochrome c from the mitochondria via a loss of the mitochondrial membrane potential (ΔΨ m ) which was associated with a increase in the ratio of B-cell lymphoma 2-associated X protein (Bax)/B cell lymphoma/leukemia-2 (Bcl-2) and activation of caspase-9 and -3. The free radical scavenger N- acetylcysteine (NAC) and caspase inhibitors markedly blocked Aloe-Emodin-induced apoptosis. Aloe-Emodin thus induced apoptosis in the SCC-4 cells through the Fas/death-receptor, mitochondria and caspase cascade. Aloe-Emodin could be a novel chemotherapeutic drug candidate for the treatment of human tongue squamous cancer in the future.

  • Aloe-Emodin affects the levels of cytokines and functions of leukocytes from Sprague-Dawley rats.
    In vivo (Athens Greece), 2006
    Co-Authors: Jack Kai Sheng Chan, Te Chun Hsia, Song Shei Lin, Ssu-ching Chen, Yung Hsien Chang, Jing Gung Chung
    Abstract:

    Aloe-Emodin has shown anti-neoplastic activity against some human cancer cell lines. This study aimed to explore the effects of Aloe-Emodin on the phagocytosis of macrophages, the activity of natural killer (NK) cells and the expression of cytokines in leukocytes from Sprague-Dawley rats. Leukocytes were collected, placed into culture plates and the functions of macrophages and NK cells and the percentage of viable cells were determined by flow cytometric analysis. Incubation of leukocytes with various concentrations of Aloe- Emodin caused a dose-dependent decrease of viable cells, a decrease of phagocytosis by macrophages, and a decrease of the activity of NK cells. Evaluation of cytokines in leukocytes by ELISA indicated that Aloe-Emodin increased the levels of interleukin (IL)-1‚ and tumor necrosis factor (TNF)-·. The results were also confirmed by PCR assay for the mRNA expression of the examined cytokines. There is much evidence that inflammatory responses are associated with cytokines which are released from leukocytes. Cytokines are soluble hormone-like protein mediators, produced by diverse cell types in response to various stimuli including other cytokines. The most important cytokine activities are associated with the immune response, inflammation, tissue injury or repair, and organ dysfunction (1-4). Aloe-Emodin (1,8-dihydroxy-3-(hydroxymethyl)-anthra- quinone) (AE) is an active component from the roots and rhizomes of Rheum palmatum and is also naturally present

  • Aloe Emodin induced in vitro g2 m arrest of cell cycle in human promyelocytic leukemia hl 60 cells
    Food and Chemical Toxicology, 2004
    Co-Authors: Hsin-chun Chen, Wen Tsong Hsieh, W. C. Chang, Jing Gung Chung
    Abstract:

    Abstract In this study, we have evaluated the chemopreventive role of Aloe-Emodin in human promyelocytic leukemia HL-60 cells in vitro by studying the regulation of proliferation, cell cycle and apoptosis. Aloe-Emodin inhibited cell proliferation and induced G2/M arrest and apoptosis in HL-60 cells. Investigation of the levels of cyclins B1, E and A by immunoblot analysis showed that cyclin E level was unaffected, whereas cyclin B1 and A levels increased with Aloe-Emodin in HL-60 cells. Investigation of the levels of cyclin-dependent kinases, Cdk1 and 2, showed increased levels of Cdk1 but the levels of Cdk2 were not effected with Aloe-Emodin in HL-60 cells. The levels of p27 were increased after HL-60 cells were cotreated with various concentrations of Aloe-Emodin. The increase of the levels of p27 may be the major factor for Aloe-Emodin to cause G2/M arrest in these examined cells. Flow cytometric assays and DNA fragmentation gel electrophoresis also confirmed Aloe-Emodin induced apoptosis in HL-60 cells. The levels of caspase-3 were increased after HL-60 cells were cotreated with 10 μM Aloe-Emodin for 12, 24, 48, and 72 hours. Taken together, Aloe-Emodin therefore appears to exert its anticarcinogenesis properties by inhibiting proliferation and inducing cell cycle arrest and apoptosis underwent activation of caspase-3 in human leukemia HL-60 cells.

  • Aloe-Emodin induced in vitro G2/M arrest of cell cycle in human promyelocytic leukemia HL-60 cells.
    Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association, 2004
    Co-Authors: Hsin-chun Chen, Wen Tsong Hsieh, W. C. Chang, Jing Gung Chung
    Abstract:

    Abstract In this study, we have evaluated the chemopreventive role of Aloe-Emodin in human promyelocytic leukemia HL-60 cells in vitro by studying the regulation of proliferation, cell cycle and apoptosis. Aloe-Emodin inhibited cell proliferation and induced G2/M arrest and apoptosis in HL-60 cells. Investigation of the levels of cyclins B1, E and A by immunoblot analysis showed that cyclin E level was unaffected, whereas cyclin B1 and A levels increased with Aloe-Emodin in HL-60 cells. Investigation of the levels of cyclin-dependent kinases, Cdk1 and 2, showed increased levels of Cdk1 but the levels of Cdk2 were not effected with Aloe-Emodin in HL-60 cells. The levels of p27 were increased after HL-60 cells were cotreated with various concentrations of Aloe-Emodin. The increase of the levels of p27 may be the major factor for Aloe-Emodin to cause G2/M arrest in these examined cells. Flow cytometric assays and DNA fragmentation gel electrophoresis also confirmed Aloe-Emodin induced apoptosis in HL-60 cells. The levels of caspase-3 were increased after HL-60 cells were cotreated with 10 μM Aloe-Emodin for 12, 24, 48, and 72 hours. Taken together, Aloe-Emodin therefore appears to exert its anticarcinogenesis properties by inhibiting proliferation and inducing cell cycle arrest and apoptosis underwent activation of caspase-3 in human leukemia HL-60 cells.

  • Aloe-Emodin effects on arylamine N-acetyltransferase activity in the bacterium Helicobacter pylori
    Planta medica, 1998
    Co-Authors: Hwang H. Wang, Jing Gung Chung, Shih H. Chang
    Abstract:

    Arylamine N-acetyltransferase (NAT) activities with p-aminobenzoic acid (PABA) and 2-aminofluorene (AF) were determined in H. pylori collected from peptic ulcer patients. Cytosols or suspensions of H. pylori with or without different concentrations of Aloe-Emodin co-treatment showed different percentages of AF and PABA acetylation. The data indicate that there was decreased NAT activity associated with increased Aloe-Emodin in H. pylori cytosols. Inhibition of growth study from H. pylori demonstrated that Aloe-Emodin elicited dose-dependent growth inhibition in H. pylori cultures. The report is the first finding of Aloe-Emodin inhibition of arylamine NAT activity in a strain of H. pylori.

Hong-zin Lee - One of the best experts on this subject based on the ideXlab platform.

  • Photodynamic activity of Aloe-Emodin induces resensitization of lung cancer cells to anoikis.
    European journal of pharmacology, 2010
    Co-Authors: Hong-zin Lee, Wen-hui Yang, Mann-jen Hour, Wen-huang Peng, Bo-ying Bao, Ping-hsiu Han, Da-tian Bau
    Abstract:

    Aloe-Emodin was found to be a photosensitizer and possess anti-tumor activity. However, the detailed mechanism underlying the biological effects of Aloe-Emodin remains unknown. In this study, we explored the mechanisms of photocytotoxicity induced by Aloe-Emodin in lung cancer H460 cells. According to the results of the photoactivated Aloe-Emodin-induced disruption of cytoskeleton, we verify that Aloe-Emodin with irradiation induces anoikis of H460 cells. Photosensitized Aloe-Emodin-induced anoikis is associated with the protein expression of α-actinin and mitogen-activated protein (MAP) kinase members. In this study, a rapid opening of the mitochondrial permeability transition pore and the change in apoptosis-related protein expression were involved in photoactivated Aloe-Emodin-induced cell death. We also demonstrated that anoikis induced by Aloe-Emodin with irradiation is mediated through the intrinsic and extrinsic death pathways in a caspase-dependent manner in H460 cells.

  • Chaperones are the target in Aloe-Emodin-induced human lung nonsmall carcinoma H460 cell apoptosis.
    European journal of pharmacology, 2007
    Co-Authors: Miao-ying Lai, Mann-jen Hour, Wen-hui Yang, Henry Wing-cheung Leung, Hong-zin Lee
    Abstract:

    Our previous study has demonstrated that Aloe-Emodin induced a significant change in the expression of apoptosis-related proteins in H460 cells. However, the molecular mechanisms underlying the biological effects of Aloe-Emodin still remain unknown. The present study applied 2D electrophoresis (pH range 4-7) to the proteins involved in Aloe-Emodin (40 muM)-induced H460 cell apoptosis. Eleven proteins were found to markedly change. These altered proteins were identified as ATP synthase, vimentin, HSP60, HSP70 and protein disulfide isomerase. Aloe-Emodin caused a time-dependent decrease in intracellular ATP levels, which might be related to direct inhibition of ATP synthase. We also observed that the activity of mitochondria was injured by Aloe-Emodin. These data clearly demonstrated that mitochondria may play a critical role in Aloe-Emodin-induced H460 cell death. Many reports emphasize that chaperones have a complex role in apoptosis. The present study suggested that the increasing protein expression of HSP60, HSP70, 150 kDa oxygen-regulated protein and protein disulfide isomerase is involved in Aloe-Emodin-induced H460 cell apoptosis. HSP70, 150 kDa oxygen-regulated protein and protein disulfide isomerase are endoplasmic reticulum chaperone. Therefore, we hypothesized that the increasing endoplasmic reticulum stress serves to promote H460 cell apoptosis after treatment with Aloe-Emodin. We also demonstrated Aloe-Emodin-induced H460 cell death through caspase-3 apoptotic pathway, but not apoptosis-inducing factor apoptotic pathway.

  • Aloe-Emodin induced DNA damage through generation of reactive oxygen species in human lung carcinoma cells.
    Cancer letters, 2005
    Co-Authors: Hong-zin Lee, Wen-hui Yang, Ching-ju Lin, Wing-cheung Leung, Shen-pen Chang
    Abstract:

    The DNA aggregation was found in Aloe-Emodin-induced H460 cell apoptosis in this study. Aloe-Emodin (40microM)-induced DNA single strand breaks were observed by comet assay. Aloe-Emodin induced decreases in the mRNA of DNA repair enzymes such as hMTH1, hOGG1 and APE. Although the activity of the radical-scavenging enzyme SOD was enhanced by Aloe-Emodin, the effects of Aloe-Emodin on H460 cell apoptosis were suspected to result from the prooxidant. These results suggest that Aloe-Emodin induced DNA damage through generation of reactive oxygen species in human lung carcinoma cells.

  • Release of nucleophosmin from the nucleus: Involvement in Aloe-Emodin-induced human lung non small carcinoma cell apoptosis.
    International journal of cancer, 2005
    Co-Authors: Hong-zin Lee, Shen-peng Chang
    Abstract:

    Aloe-Emodin (1,8-dihydroxy-3-(hydroxymethyl)-anthraquinone) is one of the active constituents from the root and rhizome of Rheum palmatum. Our previous study has demonstrated that Aloe-Emodin induced a significant change in the expression of lung cancer cell apoptosis-related proteins compared to those of control cells. However, the molecular mechanisms underlying the biological effects of Aloe-Emodin still remain unknown. Based on these reasons, we were interested in the change of Aloe-Emodin–induced total protein expression by the proteomics technique during Aloe-Emodin–induced lung cancer cell apoptosis. Our study applied 2D electrophoresis to analyze the proteins involved in Aloe-Emodin–induced apoptosis in H460 cells. We found that the release of nucleophosmin from the nucleus to the cytosol and the degradation of nucleophosmin were associated with Aloe-Emodin–induced H460 cell apoptosis. Our study also demonstrated that the gene expression of nucleophosmin remained unchanged after treatment with Aloe-Emodin. The Aloe-Emodin–caused increase in the amount of proform and fragment of nucleophosmin in cytoplasm may be one of the important events for Aloe-Emodin–induced H460 cell apoptosis. © 2004 Wiley-Liss, Inc.

  • Signaling pathway for Aloe-Emodin-induced apoptosis in human H460 lung nonsmall carcinoma cell.
    International journal of cancer, 2003
    Co-Authors: Feng-tsgh Yeh, Hong-zin Lee
    Abstract:

    Aloe-Emodin (1,8-dihydroxy-3-(hydroxymethyl)-anthraquinone) is an active component from the root and rhizome of Rheum palmatum that has been reported to exhibit antitumor effects through an unknown mechanism. Our study investigated the mechanisms of Aloe-Emodin-induced cell death in the human lung nonsmall cell carcinoma cell line H460. Aloe-Emodin (40 μM)-induced apoptosis of H460 cells involves modulation of cAMP-dependent protein kinase, protein kinase C, Bcl-2, caspase-3 and p38 protein expression. The relationship of various signals involved in cell death, such as cAMP-dependent protein kinase, protein kinase C, Bcl-2, caspase-3 and p38, has been investigated in the regulation of apoptotic cell death of Aloe-Emodin. We demonstrated that the expression of p38 is an important determinant of apoptotic death induced by Aloe-Emodin. © 2003 Wiley-Liss, Inc.

Bin Zhang - One of the best experts on this subject based on the ideXlab platform.

  • Aloe-Emodin induces apoptosis in human oral squamous cell carcinoma SCC15 cells.
    BMC complementary and alternative medicine, 2018
    Co-Authors: Jun Wen, Yao Shu, Hongxing Chu, Bin Zhang
    Abstract:

    Oral and pharyngeal cancer is the most common malignant human cancers. Chemotherapy is an effective approach for anti-oral cancer therapy, while the drug tolerance and resistance remain a problem for oral cancer patients. Aloe-Emodin, rhein and physcion are classified as anthraquinones, which are the main pharmacodynamic ingredients of Rheum undulatum L.. This study was undertaken to investigate whether Aloe-Emodin, rhein and physcion show inhibiting growth and inducing apoptosis in oral squamous cell carcinoma SCC15 cells. We found that Aloe-Emodin show inhibiting growth and inducing apoptosis in oral squamous cell carcinoma SCC15 cells, we also investigated the underlying mechanisms of apoptosis induced by Aloe-Emodin. Thiazolyl blue tetrazolium bromide (MTT) test was used to detect cell proliferation. Cell apoptosis was detected by flow cytometry. We also used western blot analysis to detect the potential mechanisms of apoptosis. Aloe-Emodin, rhein and physcion inhibit the proliferation of SCC15 cells and the order of inhibition level are Aloe-Emodin > Rhein > Physcion, the half maximal inhibitory concentrations (IC50) value of Aloe-Emodin was 60.90 μM at 48 h of treatment. Aloe-Emodin treatment resulted in a time- and dose-dependent decrease in cell viability and increased the apoptotic cell ratio. The results of western blotting showed the expression levels of caspase-9 and caspase-3 proteins increased following Aloe-Emodin treatment. Our results revealed that Aloe-Emodin treatment could inhibit cell viability of SCC15 cells and the potential mechanism of inhibition might be through the induction of apoptosis by regulation of the expression levels of caspase-9 and caspase-3. This indicates that Aloe-Emodin may be a good agent for anti-oral cancer drug exploring.

  • Aloe-Emodin induces apoptosis in human oral squamous cell carcinoma SCC15 cells
    BMC, 2018
    Co-Authors: Jun Wen, Yao Shu, Hongxing Chu, Bin Zhang
    Abstract:

    Abstract Background Oral and pharyngeal cancer is the most common malignant human cancers. Chemotherapy is an effective approach for anti-oral cancer therapy, while the drug tolerance and resistance remain a problem for oral cancer patients. Aloe-Emodin, rhein and physcion are classified as anthraquinones, which are the main pharmacodynamic ingredients of Rheum undulatum L.. This study was undertaken to investigate whether Aloe-Emodin, rhein and physcion show inhibiting growth and inducing apoptosis in oral squamous cell carcinoma SCC15 cells. We found that Aloe-Emodin show inhibiting growth and inducing apoptosis in oral squamous cell carcinoma SCC15 cells, we also investigated the underlying mechanisms of apoptosis induced by Aloe-Emodin. Methods Thiazolyl blue tetrazolium bromide (MTT) test was used to detect cell proliferation. Cell apoptosis was detected by flow cytometry. We also used western blot analysis to detect the potential mechanisms of apoptosis. Results Aloe-Emodin, rhein and physcion inhibit the proliferation of SCC15 cells and the order of inhibition level are Aloe-Emodin > Rhein > Physcion, the half maximal inhibitory concentrations (IC50) value of Aloe-Emodin was 60.90 μM at 48 h of treatment. Aloe-Emodin treatment resulted in a time- and dose-dependent decrease in cell viability and increased the apoptotic cell ratio. The results of western blotting showed the expression levels of caspase-9 and caspase-3 proteins increased following Aloe-Emodin treatment. Conclusions Our results revealed that Aloe-Emodin treatment could inhibit cell viability of SCC15 cells and the potential mechanism of inhibition might be through the induction of apoptosis by regulation of the expression levels of caspase-9 and caspase-3. This indicates that Aloe-Emodin may be a good agent for anti-oral cancer drug exploring

Hsin-chun Chen - One of the best experts on this subject based on the ideXlab platform.

  • Aloe Emodin induced in vitro g2 m arrest of cell cycle in human promyelocytic leukemia hl 60 cells
    Food and Chemical Toxicology, 2004
    Co-Authors: Hsin-chun Chen, Wen Tsong Hsieh, W. C. Chang, Jing Gung Chung
    Abstract:

    Abstract In this study, we have evaluated the chemopreventive role of Aloe-Emodin in human promyelocytic leukemia HL-60 cells in vitro by studying the regulation of proliferation, cell cycle and apoptosis. Aloe-Emodin inhibited cell proliferation and induced G2/M arrest and apoptosis in HL-60 cells. Investigation of the levels of cyclins B1, E and A by immunoblot analysis showed that cyclin E level was unaffected, whereas cyclin B1 and A levels increased with Aloe-Emodin in HL-60 cells. Investigation of the levels of cyclin-dependent kinases, Cdk1 and 2, showed increased levels of Cdk1 but the levels of Cdk2 were not effected with Aloe-Emodin in HL-60 cells. The levels of p27 were increased after HL-60 cells were cotreated with various concentrations of Aloe-Emodin. The increase of the levels of p27 may be the major factor for Aloe-Emodin to cause G2/M arrest in these examined cells. Flow cytometric assays and DNA fragmentation gel electrophoresis also confirmed Aloe-Emodin induced apoptosis in HL-60 cells. The levels of caspase-3 were increased after HL-60 cells were cotreated with 10 μM Aloe-Emodin for 12, 24, 48, and 72 hours. Taken together, Aloe-Emodin therefore appears to exert its anticarcinogenesis properties by inhibiting proliferation and inducing cell cycle arrest and apoptosis underwent activation of caspase-3 in human leukemia HL-60 cells.

  • Aloe-Emodin induced in vitro G2/M arrest of cell cycle in human promyelocytic leukemia HL-60 cells.
    Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association, 2004
    Co-Authors: Hsin-chun Chen, Wen Tsong Hsieh, W. C. Chang, Jing Gung Chung
    Abstract:

    Abstract In this study, we have evaluated the chemopreventive role of Aloe-Emodin in human promyelocytic leukemia HL-60 cells in vitro by studying the regulation of proliferation, cell cycle and apoptosis. Aloe-Emodin inhibited cell proliferation and induced G2/M arrest and apoptosis in HL-60 cells. Investigation of the levels of cyclins B1, E and A by immunoblot analysis showed that cyclin E level was unaffected, whereas cyclin B1 and A levels increased with Aloe-Emodin in HL-60 cells. Investigation of the levels of cyclin-dependent kinases, Cdk1 and 2, showed increased levels of Cdk1 but the levels of Cdk2 were not effected with Aloe-Emodin in HL-60 cells. The levels of p27 were increased after HL-60 cells were cotreated with various concentrations of Aloe-Emodin. The increase of the levels of p27 may be the major factor for Aloe-Emodin to cause G2/M arrest in these examined cells. Flow cytometric assays and DNA fragmentation gel electrophoresis also confirmed Aloe-Emodin induced apoptosis in HL-60 cells. The levels of caspase-3 were increased after HL-60 cells were cotreated with 10 μM Aloe-Emodin for 12, 24, 48, and 72 hours. Taken together, Aloe-Emodin therefore appears to exert its anticarcinogenesis properties by inhibiting proliferation and inducing cell cycle arrest and apoptosis underwent activation of caspase-3 in human leukemia HL-60 cells.

Wen Tsong Hsieh - One of the best experts on this subject based on the ideXlab platform.

  • Aloe Emodin induced in vitro g2 m arrest of cell cycle in human promyelocytic leukemia hl 60 cells
    Food and Chemical Toxicology, 2004
    Co-Authors: Hsin-chun Chen, Wen Tsong Hsieh, W. C. Chang, Jing Gung Chung
    Abstract:

    Abstract In this study, we have evaluated the chemopreventive role of Aloe-Emodin in human promyelocytic leukemia HL-60 cells in vitro by studying the regulation of proliferation, cell cycle and apoptosis. Aloe-Emodin inhibited cell proliferation and induced G2/M arrest and apoptosis in HL-60 cells. Investigation of the levels of cyclins B1, E and A by immunoblot analysis showed that cyclin E level was unaffected, whereas cyclin B1 and A levels increased with Aloe-Emodin in HL-60 cells. Investigation of the levels of cyclin-dependent kinases, Cdk1 and 2, showed increased levels of Cdk1 but the levels of Cdk2 were not effected with Aloe-Emodin in HL-60 cells. The levels of p27 were increased after HL-60 cells were cotreated with various concentrations of Aloe-Emodin. The increase of the levels of p27 may be the major factor for Aloe-Emodin to cause G2/M arrest in these examined cells. Flow cytometric assays and DNA fragmentation gel electrophoresis also confirmed Aloe-Emodin induced apoptosis in HL-60 cells. The levels of caspase-3 were increased after HL-60 cells were cotreated with 10 μM Aloe-Emodin for 12, 24, 48, and 72 hours. Taken together, Aloe-Emodin therefore appears to exert its anticarcinogenesis properties by inhibiting proliferation and inducing cell cycle arrest and apoptosis underwent activation of caspase-3 in human leukemia HL-60 cells.

  • Aloe-Emodin induced in vitro G2/M arrest of cell cycle in human promyelocytic leukemia HL-60 cells.
    Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association, 2004
    Co-Authors: Hsin-chun Chen, Wen Tsong Hsieh, W. C. Chang, Jing Gung Chung
    Abstract:

    Abstract In this study, we have evaluated the chemopreventive role of Aloe-Emodin in human promyelocytic leukemia HL-60 cells in vitro by studying the regulation of proliferation, cell cycle and apoptosis. Aloe-Emodin inhibited cell proliferation and induced G2/M arrest and apoptosis in HL-60 cells. Investigation of the levels of cyclins B1, E and A by immunoblot analysis showed that cyclin E level was unaffected, whereas cyclin B1 and A levels increased with Aloe-Emodin in HL-60 cells. Investigation of the levels of cyclin-dependent kinases, Cdk1 and 2, showed increased levels of Cdk1 but the levels of Cdk2 were not effected with Aloe-Emodin in HL-60 cells. The levels of p27 were increased after HL-60 cells were cotreated with various concentrations of Aloe-Emodin. The increase of the levels of p27 may be the major factor for Aloe-Emodin to cause G2/M arrest in these examined cells. Flow cytometric assays and DNA fragmentation gel electrophoresis also confirmed Aloe-Emodin induced apoptosis in HL-60 cells. The levels of caspase-3 were increased after HL-60 cells were cotreated with 10 μM Aloe-Emodin for 12, 24, 48, and 72 hours. Taken together, Aloe-Emodin therefore appears to exert its anticarcinogenesis properties by inhibiting proliferation and inducing cell cycle arrest and apoptosis underwent activation of caspase-3 in human leukemia HL-60 cells.