• Journal of Korea Entertainment Industry Association
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• v.13 no.1
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• pp.217-223
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• 2019

Colon cancer is the most common form of cancer diagnosis in worldwide. There are growing interests in the health benefits associated with consumption of fruits and vegetables, especially for the prevention of cancer, cardiovascular or other chronic diseases. The objective of the present study was to investigate the antioxidant and anticancer activities of natural product, guarana(GR) and graviola(GV) in human colon carcinoma HCT-116 cells. MTT assay, flow cytometry analysis were employed to investigate the anticancer mechanism and DPPH assay was determined to the antioxidant activity to scavenge free radicals in extract of these. All two extracts showed significantly antioxidant activity at 50mg/ml of concentration. GR and GV reduced HCT-116 cell proliferation in a dose dependent manner. Specially GR treatment(96.65±3.71) also significantly increased the sub-G1 population more than GV(79.58±2.87) treatment in HCT-116 at the concentration of 10mg/ml, as shown by flow cytometry assay. Statistical analyses revealed GR and GV exhibited significantly high (P < 0.05) cytotoxicity in HCT-116. These findings indicate that GN and GV may serve as novel therapeutic agents for colon cancer treatment and future leads for drug development.

• Natural Product Sciences
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• v.28 no.3
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• pp.115-120
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• 2022

Ten compounds, consisting of neoflavonoids (1-5), isoflavonoids (6 and 7), flavanone (8), and chalcones (9 and 10) were isolated from the ethyl acetate and n-butanol-soluble fractions of the heartwood of Dalbergia melanoxylon. The chemical structures were identified on the basis of spectroscopic evidence and compared to previously reported spectra. Compounds 1-10 were evaluated for cytotoxicity against HCT116 human colorectal cancer, MDA-MB-231 human metastatic breast cancer, and A2058 human melanoma cell lines. Among them, compounds 3 and 10 showed the strongest cytotoxic activity with IC₅₀ values of 11.92±1.07 μM, 10.83±1.02 μM, and 14.37±1.02 μM, 13.62±1.09 μM against HCT116 and MDA-MB-231 cell lines, respectively. Compounds 9 and 10 also had cytotoxic activity with IC₅₀ values of 13.49±1.18 μM and 9.82±0.91 μM against A2058 cell lines, respectively. To the best our knowledge, compounds 2 and 5-10 were isolated from this source for the first time.

• Herbal Formula Science
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• v.14 no.2
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• pp.21-32
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• 2006

The purpose of this study was to investigate the effect of Imyosan on apoptosis in human colorectal cancer HCT116 cells. Phellodendron amurense Rupr. and Atratylodes lancea D.C. compose Imyosan. First of all, to study the cytotoxic effect of methanol extract of Imyosan (IMS-MeOH) on HCT116 cells, the cells were treated with various concentrations of IMS-MeOH and then cell viability was determined by XTT reduction method. IMS-MeOH reduced viability of HCT116 cells in a dose and time-dependent manner. To confirm the induction of apoptosis, the c1eavage of poly ADP-ribose polymerase (PARP), a substrate for caspase-3 and a typical sign of apoptosis, and the activation of caspase-3, procaspase-8 and procaspase-9 were examined by western blot analysis. IMS-MeOH decreased procaspase-3, procaspase-8 and procaspase-9 levels in a dose-dependent manner and induced the clevage of PARP. IMS-MeOH triggered the mitochondrial apoptotic signaling by increasing the release of cytochrome c from mitochondria to cytosol. Furthermore, IMS-MeOH also downregulated the anti-apoptotic Bcl-2 and upregulated the pro-apoptotic-Bax. Therefore, these results suggest that IMS-MeOH induced HCT1l6 cell death through the mitochondrial pathway. To explore whether the activities of caspases was required for induction of apoptosis by IMS-MeOH, caspase-3, -8, -9 activity measured by using substrates, respectively. IMS-MeOH increased caspase-3, -8, -9 activity. Co-treatment with inhibitors of caspase-3, -8, -9 and IMS-MeOH significantly blocked IMS-MeOH-triggered apoptosis in HCT1l6 cells. These results suggest that IMS-MeOH induces caspases-mediated apoptosis.

• Journal of the Korean Society of Radiology
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• v.10 no.6
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• pp.387-393
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• 2016

Tumor using the efficient concomitant radiotherapy and chemotherapy to remove, prior to surgery and, either reduce the size of the tumor after surgery, or was can be made smaller, Or excised tumor, in a way to be removed, most conventional surgical method is surgical excision surgery therapy. And methods reduce or tumor size, or smaller, chemotherapy can kill tumor is administered selectively anticancer agent which increases the radioactive susceptible to tumor cells, sensitive to susceptibility to radiation are those which make it possible to respond to, either TRAIL methods of various biological cytostatic can deform the protein, by deforming the structure of the protein help to cell death it is known. In this paper, the HCT-116 cells thought to be a cancer cell to analyze the interaction of TRAIL and radiation. Experimental results, single use of TRAIL and radiation, results were compared with the control group, it was found to have no significant effect on each cell proliferation and apoptosis. Conversely treated with TRAIL, when treated in parallel radiation, it was possible to know that the HCT-116 cells significantly apoptosis occurs, The proportion of G1 ratio G0 also was found to have increased. TRAIL conclusion is increased apoptosis radiation defensive cells can know that increased radiosensitivity, also possible to alter the cell cycle, reduce cell proliferation ability stepwise it was possible. TRAIL is increased apoptosis, decreased cell proliferative capacity, it is considered to be possible to use as a radiation sensitizer.

• Journal of Microbiology and Biotechnology
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• v.24 no.12
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• pp.1654-1663
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• 2014

To examine the effect of tumor suppressor protein p53 on the antitumor activity of 2-methoxyestradiol (2-MeO-$E_2$), 2-MeO-$E_2$-induced cell cycle changes and apoptotic events were compared between the human colon carcinoma cell lines HCT116 ($p53^{+/+}$) and HCT116 ($p53^{-/-}$). When both cell types were exposed to 2-MeO-$E_2$, a reduction in the cell viability and an enhancement in the proportions of $G_2/M$ cells and apoptotic sub-$G_1$ cells commonly occurred dose-dependently. These 2-MeO-$E_2$-induced cellular changes, except for $G_2/M$ arrest, appeared to be more apparent in the presence of p53. Immunofluorescence microscopic analysis using anti-${\alpha}$-tubulin and anti-lamin B2 antibodies revealed that after 2-MeO-$E_2$ treatment, impaired mitotic spindle network and prometaphase arrest occurred similarly in both cell types. Following 2-MeO-$E_2$ treatment, only HCT116 ($p53^{+/+}$) cells exhibited an enhancement in the levels of p53, p-p53 (Ser-15), $p21^{WAF1/CIP1}$, and Bax; however, the Bak level remained relatively constant in both cell types, and the Bcl-2 level decreased only in HCT116 ($p53^{+/+}$) cells. Additionally, mitochondrial apoptotic events, including the activation of Bak and Bax, loss of ${\Delta}{\psi}m$, activation of caspase-9 and -3, and cleavage of lamin A/C, were more dominantly induced in the presence of p53. The Bak-specific and Bax-specific siRNA approaches confirmed the necessity of both Bak and Bax activations for the 2-MeO-$E_2$-induced apoptosis in HCT116 cells. These results show that among 2-MeO-$E_2$-induced apoptotic events, including prometaphase arrest, up-regulation of Bax level, down-regulation of Bcl-2 level, activation of both Bak and Bax, and mitochondria-dependent caspase activation, the modulation of Bax and Bcl-2 levels is the target of the pro-apoptotic action of p53.

• The Korea Journal of Herbology
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• v.21 no.2
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• pp.37-46
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• 2006

Objectives : The purpose of this study was to investigate the effect of Dangguibohyultang (DB) and its combination (DB-I; Astragali membraneus BUNGE : Angelica gigas NAKAI=5:1, DB-II; Astragali membraneus BUNGE:Angelica gigas NAKAI=1:1, DB-III; Astragali membraneus BUNGE:Angelica gigas NAKAI=1:5,) on apoptosis in human colorectal adenocarcinoma HCT116 cells. Methods : To study the cytotoxic effect of methanol extract of DB-I, DB-II and DB-III on HCT116 cells, the cell viability was determined by XTT reduction method and ttypan blue exclusion assay. To confirm the induction of apoptosis, the cleavage of poly ADP-ribose polymerase (PARP), a substrate for caspase-3 and a typical sign of apoptosis, and the activation of procaspase-3, -8 and -9 were examined by western blot analysis. Furthermore, DB-induced apoptosis was confirmed by DNA fragmentation. The release of cytochrome C from mitochondria to cytosol, the level of Bcl-2 and Bax, and the expressions of Raf/MEK/ERK were examined by western blot analysis. Results : DB-I and DB-II reduced proliferation of HCT116 cells in a dose-dependent manner. DB-I and DB-II decreased procaspase-3, -8, -9 levels in a dose-dependent manner and induced the clevage of PARP. DB-I and DB-II also triggered the mitochondrial apoptotic signaling by increasing the release of cytochrome C from mitochondria to cytosol, decreasing of anti-apoptotic Bcl-2, and increasing of pro-apoptotic Bax. DB-I and DB-II decreased the activation of Ras/Raf/MEK/ERK cascade in a dose-dependent manner. Conclusion : These results suggest that DB-I and DB-II induce apoptosis via mitochondrial pathway in HCT116 cells. Furthermore, Raf/MEK/ERK cascade is involved in DB-induced apoptosis. These results suggest that DB is potentially useful as a chemotherapeutic agent in human liver cancer.

• Journal of Life Science
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• v.31 no.10
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• pp.929-936
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• 2021

In the present study, we screened candidate natural compounds which possess the strong anti-proliferative effects on human colorectal HCT116 cells using the commercial natural product library (Selleckchem, L1400) based on cell viability assay. Human colorectal cancer HCT116 cells were incubated with 50 μM of each compound from the natural product library, and then cell viability was measured by MTT assay. From the first screening, five different kinds of natural products (chrysin, diosmetin, emodin, piperlongumine, and tanshinone I) were selected based on cell viability assay in HCT116 cells and commercial availability. All selected natural products significantly decreased cell viabilities in HCT116 cells, whereas pro-apoptotic protein NAG-1 is strongly induced by chrysin or emodin treatment. Chrysin and emodin decreased cell viability in a dose-dependent manner. Moreover, chrysin and emodin increased the expression of pro-apoptotic NAG-1 protein in a dose- and time-dependent manner. In addition, PARP cleavage induced by chrysin or emodin was recovered in part by the transfection of NAG-1 siRNA indicating that NAG-1 may be one of the genes responsible for apoptosis induced by chrysin or emodin. Overall, our findings may provide basic screening data on natural products which possess anti-proliferative activities and may help to understand the molecular mechanisms of anti-proliferative and pro-apoptotic activities mediated by chrysin and emodin.

• Journal of Food Hygiene and Safety
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• v.34 no.3
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• pp.303-308
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• 2019

L-carnitine is found in high levels in muscle tissues. It has been developed as a nutrient and dietary supplement, and also used as a therapeutic supplement in various diseases including type II diabetes, osteoporosis and metabolic neuropathies. However, it is not fully understood how it affects cellular mechanisms in colorectal cancer. Therefore, we attempted to determine the effect of L-carnitine in HCT116 human colorectal cancer cells. First, the HCT116 cells were exposed to L-carnitine for 24 hours at 0-40 mM, and then analyzed for cellular proliferation, oxidative stress and related mechanisms. In a MTT assay, L-carnitine inhibited cellular proliferation and induced reactive oxygen species (ROS) in HCT116 by DCF-DA analysis. To analyze the mechanism of L-carnitine in colorectal cancer cells, we performed a western blot analysis for pERK1/2 and pp38 MAP kinase. The western blot showed that L-carnitine significantly increased protein levels of pERK1/2 and pp38 compared with control. Taken together, we found that L-carnitine has anti-proliferative function via increased ROS and activation of ERK1/2 and p38 pathway in HCT116. These findings suggest that L-carnitine may have an anti-proliferative role on colorectal cancer.

• Biomolecules & Therapeutics
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• v.32 no.1
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• pp.104-114
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• 2024

Licochalcone C (LCC; PubChem CID:9840805), a chalcone compound originating from the root of Glycyrrhiza inflata, has shown anticancer activity against skin cancer, esophageal squamous cell carcinoma, and oral squamous cell carcinoma. However, the therapeutic potential of LCC in treating colorectal cancer (CRC) and its underlying molecular mechanisms remain unclear. Chemotherapy for CRC is challenging because of the development of drug resistance. In this study, we examined the antiproliferative activity of LCC in human colorectal carcinoma HCT116 cells, oxaliplatin (Ox) sensitive and Ox-resistant HCT116 cells (HCT116-OxR). LCC significantly and selectively inhibited the growth of HCT116 and HCT116-OxR cells. An in vitro kinase assay showed that LCC inhibited the kinase activities of EGFR and AKT. Molecular docking simulations using AutoDock Vina indicated that LCC could be in ATP-binding pockets. Decreased phosphorylation of EGFR and AKT was observed in the LCC-treated cells. In addition, LCC induced cell cycle arrest by modulating the expression of cell cycle regulators p21, p27, cyclin B1, and cdc2. LCC treatment induced ROS generation in CRC cells, and the ROS induction was accompanied by the phosphorylation of JNK and p38 kinases. Moreover, LCC dysregulated mitochondrial membrane potential (MMP), and the disruption of MMP resulted in the release of cytochrome c into the cytoplasm and activation of caspases to execute apoptosis. Overall, LCC showed anticancer activity against both Ox-sensitive and Ox-resistant CRC cells by targeting EGFR and AKT, inducing ROS generation and disrupting MMP. Thus, LCC may be potential therapeutic agents for the treatment of Ox-resistant CRC cells.

• Journal of Microbiology and Biotechnology
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• v.28 no.3
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• pp.491-497
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• 2018

Lipopolysaccharide (LPS), a component of the cell wall of gram-negative bacteria, elicits the secretion of cytokines, such as interferons, that stimulate the host defense system. Previously, we demonstrated that interferons induce interferon regulatory factors (IRFs) 1, 3, and 7, which regulate the transcription of Noxa and alter the expression profiles of Bcl-2 family proteins in tumors. However, the immediate consequences of LPS stimulation on Noxa and BH3 expression in tumor cells remain uncharacterized. In this study, we determined that LPS induced Noxa expression in CT26 cells. Furthermore, studies in HCT116 parental and HCT116 p53-deficient cells revealed that LPS-mediated Noxa was independent of p53. Meanwhile, IRF1, 3, and 7 in CT26, HCT116 parental, and HT116 p53-deficient cells were upregulated by LPS stimulation, suggesting that LPS induces the expression of these IRFs in a p53-independent manner. The responsiveness of IRF1, 3, 4, and 7 binding to the Noxa promoter region to LPS indicated that IRF1, 3, and 7 activated Noxa expression, whereas IRF4 repressed Noxa expression. Together, these results suggest that LPS directly affects Noxa expression in tumor cells through IRFs, implicating that it may contribute to LPS-induced tumor regression.