• Title/Summary/Keyword: colon adenocarcinoma cells

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Chemopreventive Effect of Protein Extract of Asterina pectinifera in HT-29 Human Colon Adenocarcinoma Cells

  • Shon Yun-Hee;Nam Kyung-Soo
    • Archives of Pharmacal Research
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    • v.29 no.3
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    • pp.209-212
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    • 2006
  • We investigated the effect of protein extract of Asterina pectinifera on the activity of 4 enzymes that may playa role in adenocarcinoma of the colon: quinone reductase (QR), glutathione Stransferase (GST), ornithine decarboxylase (ODC), and cyclooxygenase (COX)-2. QR and GST activity increased in HT-29 human colon adenocarcinoma cells increased that had been exposed to 4 concentrations of the protein extract (80, 160, 200, and $240{\mu}g/mL$). Additionally, 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced ODC activity decreased significantly in cells exposed to the extract in concentrations of $160{\mu}g/mL$ (p<0.05), $200{\mu}g/mL$ (p<0.005), and $240{\mu}g/mL$ (p<0.005). TPA-induced COX-2 activity also decreased in cells exposed to extract concentrations of 10, 20, 40, and $60{\mu}g/mL$. COX-2 expression was also inhibited in cells exposed to this extract. These results suggest that this protein extract of A pectinifera has chemopreventive activity in HT-29 human colon adenocarcinoma cells, and therefore, may have the potential to function as a chemopreventive agent in human colorectal cancer.

Invitro Anticancer Effect of Chinese Cabbage Kimchi Fractions (배추김치 분획물의 in vitro 항암효과)

  • 박건영;조은주;이숙희;강갑석
    • Journal of the Korean Society of Food Science and Nutrition
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    • v.28 no.6
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    • pp.1326-1331
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    • 1999
  • In vitro anticancer effect of Chinese cabbage kimchi fractions was investigated by using human cancer cells, AGS human gastric adenocarcinoma cells and HT 29 human colon adenocarcinoma cells. The Chinese cabbage kimchi(fermented for 4 days at 15oC) was fractionated into 7 groups, methanol extract, hexane fraction(fr.), methanol soluble fr., dichloromethane fr., ethylacetate fr., butanol fr. and aqueous fr.. Chinese cabbage kimchi fractions inhibited the growth of AGS and HT 29 cancer cells as dose dependent. In particular, the dichloromethane fr. showed the highest inhibitory effect among other fractions. When the dichloromethane fr.(0.2mg/ml) was treated, the number of AGS and HT 29 survival cancer cells reduced to 12$\times$104/ml and 11$\times$104/ml compared to 166$\times$104/ml and 50$\times$104/ml of the controls, respectively. Chinese cabbage kimchi fractions also inhibited the DNA synthesis of the cancer cells. They inhibited the DNA synthesis of AGS human gastric adenocarcinoma cells more efficiently than that of HT 29 human colon adenocarcinoma cells. These results indicate that Chinese cabbage kimchi fractions show in vitro anticancer activity and the dichloromethane fr. among them reveals the highest effect.

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Chemopreventive effects of polysaccharides extract from Asterina pectinifera on HT-29 human colon adenocarcinoma cells

  • Nam, Kyung-Soo;Shon, Yun-Hee
    • BMB Reports
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    • v.42 no.5
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    • pp.277-280
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    • 2009
  • We examined the effects of polysaccharides extracted from Asterina pectinifera on the activities of quinone reductase (QR), glutathione S-transferase (GST), ornithine decarboxylase (ODC), cyclooxygenase (COX)-2 and glutathione (GSH) levels in HT-29 human colon adenocarcinoma cells. We found that the polysaccharides extract induced QR activity in a dose-dependent manner over a concentration range of $20-60\;{\mu}g/ml$ and increased GST activity as much as 1.4-fold over controls. GSH levels were increased 1.3- and 1.5-fold with the extract at 40 and $60\;{\mu}g/ml$, respectively. The activity and protein expression of ODC in 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced colon cancer cells was inhibited by the extract. The polysaccharides suppressed TPA-induced prostaglandin (PG) production. These data indicate that polysaccharides from A. pectinifera increase phase II detoxification enzyme activity and inhibit ODC and COX-2 activities in HT-29 human colon adenocarcinoma cells. Consequently, this effect may contribute to the protective effect of polysaccharides from A. pectinifera against colon cancer.

Heptaphylline Induces Apoptosis in Human Colon Adenocarcinoma Cells through Bid and Akt/NF-κB (p65) Pathways

  • Boonyarat, Chantana;Yenjai, Chavi;Vajragupta, Opa;Waiwut, Pornthip
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.23
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    • pp.10483-10487
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    • 2015
  • Heptaphylline derivatives are carbazoles in Clausena harmandiana, a medicinal plant that is utilized for headache, stomach ache, and other treatments of illness. The present study examined the effects of heptaphylline and 7-methoxyheptaphylline on apoptosis of human colon adenocarcinoma cells (HT-29 cell line). Quantification of cell viability was performed using cell proliferation assay (MTT assay) and of protein expression through immunoblotting. The results showed that only heptaphylline, but not 7-methoxyheptaphylline, significantly significantly activated cleaved of caspase-3 and poly (ADP-ribose) polymerase (PARP-1) which resulted in HT-29 cell death. We found that heptaphylline activated BH3 interacting-domain death agonist (Bid) and Bak, proapoptotic proteins. In contrast, it suppressed X-linked inhibitor-of-apoptosis protein (XIAP), Bcl-xL and survivin, inhibitors of apoptosis. In addition, heptaphylline inhibited activation of NF-${\kappa}B$/p65 (rel), a regulator of apoptotic regulating proteins by suppressing the activation of Akt and $IKK{\alpha}$, upstream regulators of p65. The findings suggested that heptaphylline induces apoptosis in human colon adenocarcinoma cells.

Effects of Duchesnea Indica of Colorectal Adenocarcinoma Cells (사매가 대장암 세포에 미치는 영향)

  • Lee, Do-Hyoung;Kim, Jin-Sung;Yoon, Sang-Hyub;Ryu, Ki-Won;Ryu, Bong-Ha
    • The Journal of Internal Korean Medicine
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    • v.26 no.2
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    • pp.310-319
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    • 2005
  • Objectives: The aim is to identify any anti-tumor effects of Duchesnea indica(Andr.) Focke on colon cancer cells. Materials & Methods: Colo201 human adenocarcinoma cells were obtained from American Type Culture Collection. The boiled extract of Duchesnea indica(Andr.) Focke was added (10 and 20 microliters) to cultures and observed at 0, 6, and 12 hours, and at 12-hour intervals thereafter. Morphological changes in colon cancer cells were observed through an inverted microscope, Destruction of colon cancer cells was measured through Trypan blue exclusion testing. Suppression of the viability of colon cancer cells were measured via MTT assay. Anti-cancer mechanisms in the cell cycle of colon cancer cells were analysed via flow cytometry. Results: After introduction of Duchesnea indica(Andr.) Focke to cultures several changes were seen. Significant atrophy of the nucleus and cytoplasm of colon cancer cells was observed, indicating cell injury. Destruction of colon cancer cells was observed in direct proportion to dosage and duration. Suppression of viability of colon cancer cells for each test group was greater than that of the control group increasingly over time(36h, 48h, 60h, 72h), which was statistical significant (p<0.05). Cell numbers of the mitosis phase of the colon cancer cell cycle reduced. Conclusions: Statistcally significant anti-tumor effects of Duchesnea indica(Andr.) Focke were observed in this in vitro experiment. Results support a role for Duchesnea indica(Andr.) Focke in treatment of colon cancer. though it will required progressive research to develop a practical treatment.

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Role of Intracellular Calcium in Clotrimazole-Induced Alteration of Cell Cycle Inhibitors, p53 and p27, in HT29 Human Colon Adenocarcinoma Cells

  • Thapa, Dinesh;Kwon, Jun-Bum;Kim, Jung-Ae
    • Biomolecules & Therapeutics
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    • v.16 no.1
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    • pp.21-27
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    • 2008
  • Clotrimazole (CLT), a potent antifungal drug, is known to inhibit tumor cell proliferation. In the present study, we examined the role of intracellular $Ca^{2+}$ in CLT-induced cell cycle arrest of colon adenocarcinoma HT29 cells. CLT inhibited growth of HT29 cells in a concentration-dependent manner, which was associated with inhibition of cell cycle progression at the G(1)-S phase transition and an increase in the expression of cell cycle inhibitor proteins p27 and p53. CLT also suppressed the $Ca^{2+}$ overload by A23187, a calcium ionophore, suggesting its role in modulation of intracellular $Ca^{2+}$ concentration in HT29 cells. The simultaneous application of CLT and A23187 with addition of $CaCl_2$ (1mM) to the medium significantly reversed CLT-induced p27 and p53 protein level increase and growth suppression. Our results suggest that CLT induces cell cycle arrest of colon adenocarcinoma HT29 cells via induction of p27 and p53, which may, at least in part, be mediated by alteration of intracellular $Ca^{2+}$ level.

Glutaraldehyde-Mediated Synthesis of Asparaginase-Bound Maghemite Nanocomposites: Cytotoxicity against Human Colon Adenocarcinoma Cells

  • Baskar, G;George, Garrick Bikku
    • Asian Pacific Journal of Cancer Prevention
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    • v.17 no.9
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    • pp.4237-4240
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    • 2016
  • Drugs processed using nanobiotechnology may be more biocompatible, with sustainable and stabilised release or action. L-asparaginase produced from fungi has many advantages for treatment of lymphocytic leukemia with lesser side effect. In the present work, maghemite nanobiocomposites of fungal asparaginase were produced using glutaraldehyde-pretreated colloidal magnetic nanoparticles. Formation of nanobiocomposites was observed using laser light scattering and confirmed by UV-visible spectrophotometry with the absorption peak at 497 nm. The specific asparaginase activity was increased from 320 U/mg with crude asparaginase to 481.5 U/mg. FTIR analysis confirmed that primary amines are the functional groups involved in binding of asparaginase on magnetic nanoparticles. The average size of the produced nanobiocomposite was found in the range of 30 nm to 40 nm using histogram analysis. The magnetic nanobiocomposite of asparaginase synthesised using glutaraldehyde showed 90.75% cytotoxicity against human colon adenocarcinoma cell lines. Hence it can be used as an active anticancer drug with an augmented level of bioavailability.

The Effects of Korean Traditional Medicine Mixture on Cytokine Level, Food Intake and Nutrition Metabolism of the Cachexia Induced-Mice (혼합한약재가 악액질이 유도된 생쥐의 Cytokine분비 및 식이섭취와 영양대사에 미치는 영향)

  • 왕수경;윤은영;박정민;임종순;김승형
    • Journal of Nutrition and Health
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    • v.36 no.4
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    • pp.368-375
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    • 2003
  • Cancer cachexia, characterized by weight loss and progressive tissue wasting, has been postulated to be mediated by cytokines. This study was conducted to evaluate the effect of Korean Traditional Medicine (KTM ; mokhyang, jisil, osooyu) mixture on food intake, blood cytokines level and blood nutrients status of the cachexia induced-mice. Thirty male Balb/c mice aged 6-8 weets were blocked into 3 groups that were Normal (no colon26 cells) Control (colon 26 cells) and KTM (colon26 cells + KTM extract mixture) group. In Control and KTM groups, murine adenocarcinoma colon 26 cells were injected subcutaneously to induce cachexia. KTM mice were given 200 ul KTM extract mixture (7%) per day. Half of each groups were sacrificed at the 14 th day to see serum cytokines & nutrients and the others were fed until almost of control group died to see life span. food intake and body weight were decreased significantly in cachexia induced groups. Tumor weight of KTM group was significantly lower than control group. Serum cytokines (IL-1$\beta$ and TNF-$\alpha$) level of cachexia induced groups were increased than those of normal group, and those of KTM group were significantly lower than the level of control group. Total serum protein and serum albumin were higher in KTM group than other groups. TG and fatty acid were lower in cachexia induced groups than normal group. HDL-cholesterol in serum was increased in KTM group. Effect of oral administration of KTM extract mixture on survival time of colon26 bearing mice showed extension of the life span. Overall, this study showed that KTM (mokhyang, jisil, osooyu) extract mixture inhibited the growth of cancer cell, changed the secretion of cytokines induced by colon26 adenocarcinoma in mice, and changed nutrition metabolism.

Fine Needle Aspiration Cytology of Metastatic Adenocarcinoma of the Thyroid Gland from the Colon - Report of a Case - (갑상선으로 전이된 대장선암종의 세침흡인 세포학적 소견 - 1예 보고 -)

  • Kim, Sook;Jin, So-Young;Lee, Dong-Wha
    • The Korean Journal of Cytopathology
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    • v.5 no.1
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    • pp.41-45
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    • 1994
  • Most common metastatic tumors of the thyroid gland are squamous cell carcinoma of head and neck region, adenocarcinoma of breast and lung, malignant melanoma, and renal cell carcinoma of kidney in order of frequency. Metastasis from gastrointestinal tract to the thyroid gland rarely occurs. We experienced a case of fine needle aspiraton cytology of metastatic adenocarcinoma of both thyroid glands from the colon. Cytologic smears showed picket-fence like arrangement of nuclei of carcinoma cells and syncytial type of tissue fragments with acinar pattern on necrotic or mucoid background.

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LncRNA LINC01232 Enhances Proliferation, Angiogenesis, Migration and Invasion of Colon Adenocarcinoma Cells by Downregulating miR-181a-5p

  • Yu Yuan;Zhou Long
    • Journal of Microbiology and Biotechnology
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    • v.33 no.3
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    • pp.398-409
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    • 2023
  • LncRNAs play crucial roles in the progression of colon adenocarcinoma (COAD), but the role of LINC01232 in COAD has not received much attention. The present study was designed to explore the related mechanisms of LINC01232 in the progression of COAD. LINC01232, miR-181a-5p, p53, c-myc, Bcl-2, cyclin D1, p16, Bax, VEGF, E-cadherin, vimentin, N-cadherin and SDAD1 expressions were determined by western blot and qRT-PCR. CCK-8, tubule formation, and Transwell assays were employed to detect proliferation, angiogenesis, and migration/invasion of COAD cells, respectively. The relationship between LINC01232 and miR-181a-5p was predicted by LncBase Predicted v.2, and then verified through dual luciferase reporter gene assay. According to the results, LINC01232 was highly expressed in COAD cells and enhanced proliferation, angiogenesis, migration, and invasion of COAD cells. Downregulated LINC01232 promoted expression of p53 and p16, and inhibited c-myc, Bcl-2 and cyclin D1 expressions in COAD cells, while upregulation of LINC01232 generated the opposite effects. LINC01232 was negatively correlated with miR-181a-5p while downregulated miR181a-5p could reverse the effects of siLINC01232 on cell proliferation, angiogenesis, migration, and invasion. Similarly, miR-181a-5p mimic could also offset the effect of LINC01232 overexpression. SiLINC01232 increased the expressions of Bax and E-cadherin, and decreased the expressions of VEGF, vimentin, N-cadherin and SDAD1, which were partially attenuated by miR-181a-5p inhibitor. Collectively, LINC01232 enhances the proliferation, migration, invasion, and angiogenesis of COAD cells by decreasing miR-181a-5p expression.