• Journal of the Korean Society of Food Science and Nutrition
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• v.33 no.4
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• pp.633-640
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• 2004

This study was performed to investigate the cytotoxic effect of the water-extract from Chaga mushroom (Inonotus obliquus) compositions containing powdered green tea in HCT-15 human colon carcinoma, AGS human gastric carcinoma and NIH3T3 mouse normal fibroblast cells using viable cell count and MTT assay. The water-extract from Chaga mushroom compositions induced inhibitory effects on proliferation of HCT-15 and AGS cells in the MTT assay and viable cell count. However, mouse normal NIH3T3 cells were exhibited 80% survival under the same condition. Chaga mushroom compositions showed highly antiproliferative effect in human cancer cell line HCT-15 and AGS, but not in mouse normal cell line NIH3T3. These results suggest that Chaga mushroom (Inonotus obliquus) compositions containing powdered green tea are the candidate for chemoprevention in colon and gastric cancer.

• Journal of Life Science
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• v.17 no.5 s.85
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• pp.671-677
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• 2007

This study was performed to investigate the effect of the water-extract from non-fermented or fermented Chaga mushrooms (Inonotus obliquus) on the proliferation and apoptosis of the NIH3T3 mouse normal fibroblast cells and various human cancer cell lines including HCT-15 human colon carcinoma, AGS human gastric carcinoma, MCF-7 human breast adenocarcinoma, Hep3B human hepatocellular carcinoma and HeLa human cervical carcinoma using MTT(3-[4,5-dimethylthiazol-2-yl] -2,5-diphenyl tetrazolium bromide) assay and DNA fragmentation. In an anti-cancer test using various human cancer cells, fermented Chaga mushroom extract showed higher antiproliferating effect than that of non-fermented Chaga mushroom extract. Mouse normal NIH3T3 cells were exhibited 80% above survival under fermented or non-fermented Chngn mushroom extract of various concentrations(0, 0.5 and 1 mg/ml). Fermented Chaga mushroom extract significantly inhibited cell growth on HCT-15 cells in a dose-dependent manner. HCT-15 cells treated with non-fermented or fermented Chaga mushrooms extract produced a distinct oligonucleosomal ladder with different sizes of DNA fragments, a typical characteristic of cells undergoing apoptosis. These results suggest that fermented Chaga mushroom extract suppresses growth of HCT-15 human colon carcinoma cells through apoptosis.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.2
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• pp.617-622
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• 2014

Voacanga globosa (Blanco), a plant endemic to the Philippines, is traditionally used especially by indigenous people of Bataan in the treatment of ulcers, wounds and tumorous growths. This study aimed to provide scientific evidence to therapeutic properties by determining cytotoxic and pro-apoptotic activity of HPLC fractions from leaves on HCT116 human colon carcinoma and A549 human lung carcinoma cell lines. Ethanolic extraction was performed on V globosa leaves followed by hexane and ethyl acetate partitioning. Silica gel column chromatography and high performance liquid chromatography (HPLC) produced MP1, MP2 and MP3 fractions. Cytotoxic activity of the fractions was determined through MTT assay against the cancer cell lines HCT116 and A549 and the non-cancer AA8 Chinese hamster ovarian cell line. Pro-apoptotic activities of the most active fractions were further assessed through DAPI staining, TUNEL assay and JC-1 mitochondrial membrane potential assay with HCT116 cells. While the MPI fraction exerted no significant activity against all cell lines tested, MP2 and MP3 fractions demonstrated high toxicity against HCT116 and A549 cells. The MP3 fraction induced formation of apoptotic bodies, condensed DNA and other morphological changes consistent with apoptosis of HCT116 cells and TUNEL assay showed significant increase in DNA fragmentation over time. In these cells, the MP3 fraction also induced mitochondrial membrane destabilization, which is generally associated with the beginning of apoptosis. Phytochemical analysis demonstrated the presence only of saponins and terpenoids in the MP3 fraction. The results indicate that the MP3 fraction exerts cytotoxic activity on HCT116 cells via induction of apoptosis triggered by loss of mitochondrial membrane potential crucial for cell survival.

• IMMUNE NETWORK
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• v.12 no.2
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• pp.66-69
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• 2012

The immunological death induction by EY-6 on the human tumor cell lines was screened. Human colon carcinoma (HCT15, HCT116), gastric carcinoma (MKN74, SNU668), and myeloma (KMS20, KMS26, KMS34) cells were died by EY-6 treatment with dose-dependent manner. CRT expression, a typical marker for the immunological death, was increased on the EY-6-treated colorectal and gastric cancer cells. Interestingly, the effects on the myeloma cell lines were complicated showing cell line dependent differential modulation. Cytokine secretion from the EY-6 treated tumor cells were dose and cell-dependent. IFN-${\gamma}$ and IL-12 secretion was increased in the treated cells (200% to over 1000% of non-treated control), except HCT116, SNU668 and KMS26 cells which their secretion was declined by EY-6. Data suggest the potential of EY-6 as a new type of immuno-chemotherapeutics inducing tumor-specific cell death. Further studies are planned to confirm the efficacy of EY-6 including in vivo study.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.20
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• pp.8581-8586
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• 2014

Activin is a multifunctional growth and differentiation factor of the growth factor-beta (TGF-${\beta}$) superfamily, which inhibits the proliferation of colon cancer cells. It induces phosphorylation of intracellular signaling molecules (Smads) by interacting with its type I and type II receptors. Previous studies showed that human activin receptor-interacting protein 2 (hARIP2) can reduce activin signaling by interacting with activin type II receptors; however, the activity of hARIP2 in colon cancer has yet to be detailed. In vitro, overexpression of hARIP2 reduced activin-induced transcriptional activity and enhanced cell proliferation and colony formation in human colon cancer HCT8 cells and SW620 cells. Also, hARIP2 promoted colon cancer cell apoptosis, suggesting that a vital role in the initial stage of colon carcinogenesis. In vivo, immunohistochemistry revealed that hARIP2 was expressed more frequently and much more intensely in malignant colon tissues than in controls. These results indicate that hARIP2 is involved in human colon tumorigenesis and could be a predictive maker for colon carcinoma aggressiveness.

• Journal of the Korean Chemical Society
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• v.63 no.2
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• pp.85-93
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• 2019

A panel of chalcone-sulphonamide hybrids has been designed by tethering appropriate sulphonamide scaffold with substituted chalcones as a multi-target drug for anticancer screening. Chalcones were prepared by Claisen-Schmidt condensation reaction of a substituted aldehyde with para aminoacetophenone. All the synthesized compounds were evaluated against selected five cancer cell lines, MCF-7 (Breast cancer), DU-145 (Human prostate Carcinoma), HCT-15 (Colon cancer), NCIH-522 (stage 2, adenocarcinoma; non-small cell lung cancer) and HT-3 (Human cervical cancer). Most of the synthesized chalcone-sulphonamide hybrids showed amended cytotoxic activity against various cancer cell lines which may be attributed to the linkage of sulphonamide with chalcone skeleton. The synthesized compounds were characterized by FT-IR, $^1H$ NMR, $^{13}C$ NMR and HR-LCMS and spectral study assert the structures of synthesized sulphonamide-chalcone hybrids.

• 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.

• Archives of Pharmacal Research
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• v.24 no.6
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• pp.527-531
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• 2001

Two triterpenoids, 24-methylene-3,4-seco-cycloart-4(28)-en-3-oic acid (1) and 3-oxo-$9{\beta}$-lanosta-7,22Z,24-trien-26,23-olive (6) were isolated from Abies koreana, together with $\beta$-sitosterol (2), maltol (3), ${\beta}-sitosterol-O-{$\beta}-D-glucoside$ (4), and hexacosylferulate (5). The structures of the compounds were established based on the spectroscopic data. The cytotoxic activities of triterpenoids have been evaluated using the sulforhodamine B (SRB) method. Compound 1 showed moderate cytotoxicities against human lung carcinoma (A549), ovarian carcinoma (SK-OV-3), malignant melanoma (SK-MEL-2), and colon carcinoma (HCT-15) cell lines.

• Journal of the Korean Society of Food Science and Nutrition
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• v.41 no.1
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• pp.26-32
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• 2012

Purified salt and several different types of sea salts showed comutagenicity in the presence of MNNG (N-methyl-N'-nitro-N-nitrosoguanidine). However, the salts exhibited anti-cancer effects in HCT-116 human colon carcinoma cells and AGS human gastric adenocarcinoma cells. Sea salt showed less comutagenicity effects than purified salt. French sea salt (Salines de Guerande) and Korean sea salt I, which contained higher levels of minerals, showed less comutagenicity. In MTT assay, when HCT-116 and AGS cancer cells were treated with the salts, French sea salt (36% and 34%) and Korean sea salt I (35% and 33%) showed higher anticancer activities than Spanish sea salt (33% and 31%), Italian sea salt (29% and 27%), Korean sea salt II (22% and 22%), or purified salt (18% and 15%) at a salt concentration of 1%. French sea salt and Korean sea salt I also showed better anticancer activities than the other salt samples at a low concentration of 0.5% (p<0.05). Apoptosis related genes of Bax and Bcl-2 were regulated by the treatment of the salt in the colon cancer cells. French sea salt and Korean sea salt I especially increased Bax mRNA expression, but decreased Bcl-2 expression, indicating that they can induce apoptosis of the cancer cells. From the experimental results, sea salt showed better health functional effects than the purified salt, and French sea salt and Korean sea salt I which contained high levels of Ca, K, and Mg showed better effects.

• Molecules and Cells
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• v.37 no.12
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• pp.899-906
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• 2014

Prostaglandin $E_2$ ($PGE_2$) promotes tumor-persistent inflammation, frequently resulting in cancer. Curcumin is a diphenolic turmeric that inhibits carcinogenesis and induces apoptosis. $PGE_2$ inhibits curcumin-induced apoptosis; however, the underlying inhibitory mechanisms in colon cancer cells remain unknown. The aim of the present study is to investigate the survival role of $PGE_2$ and whether addition of exogenous $PGE_2$ affects curcumininduced cell death. HCT-15 cells were treated with curcumin and $PGE_2$, and protein expression levels were investigated via Western blot. Reactive oxygen species (ROS) generation, lipid peroxidation, and intracellular glutathione (GSH) levels were confirmed using specific dyes. The nuclear factor-kappa B ($NF-{\kappa}B$) DNA-binding was measured by electrophoretic mobility shift assay (EMSA). $PGE_2$ inhibited curcumin-induced apoptosis by suppressing oxidative stress and degradation of PARP and lamin B. However, exposure of cells to the EP2 receptor antagonist, AH6809, and the PKA inhibitor, H89, before treatment with $PGE_2$ or curcumin abolished the protective effect of $PGE_2$ and enhanced curcumin-induced cell death. $PGE_2$ activates PKA, which is required for cAMP-mediated transcriptional activation of CREB. $PGE_2$ also activated the Ras/Raf/Erk pathway, and pretreatment with PD98059 abolished the protective effect of $PGE_2$. Furthermore, curcumin treatment greatly reduced phosphorylation of CREB, followed by a concomitant reduction of $NF-{\kappa}B$ (p50 and p65) subunit activation. $PGE_2$ markedly activated nuclear translocation of $NF-{\kappa}B$. EMSA confirmed the DNA-binding activities of $NF-{\kappa}B$ subunits. These results suggest that inhibition of curcumin-induced apoptosis by $PGE_2$ through activation of PKA, Ras, and $NF-{\kappa}B$ signaling pathways may provide a molecular basis for the reversal of curcumin-induced colon carcinoma cell death.