• Title/Summary/Keyword: HT-29 human colon cancer cells

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Rhanella aquatilis 유래 당단백질과 항암제 혼합물에 의한 인체 대장암 HT29세포에 대한 항암상승효과 (Synergistic Anticancer Activity of a Mixture of Anticancer Agent with Proteoglycan from Rhanella aquatilis against Human Colon Cancer Cell HT29)

  • 박혜지;김광현
    • 한국미생물·생명공학회지
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    • 제41권3호
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    • pp.379-382
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    • 2013
  • Rhanella aquatilis AY2000 균주가 생산하는 일종의 당단백질인 항효모성 물질 (AYS)에 대한 항암활성을 조사하기 위해 in vitro에서 암세포에 대한 AYS의 세포독성을 조사하였다. 그 결과 AYS는 인체의 Jurkat T 세포와 마우스의 sarcoma 180 세포에 대해서는 세포독성을 나타내지 않았으나, 인체 대장암세포인 colon cancer TH20 세포에는 세포독성을 나타내었다. 또한 이 AYS는 62.5에서 500 ${\mu}g/ml$까지 농도의존적으로 인체대장암세포에 대해 세포독성을 증가시켰다. 뿐만 아니라 이 AYS와 시판 항암제를 혼합하여 처리한 결과 시판 항암제를 단독으로 처리한 것 보다 인체대장암세포에 대한 항암효과가 더욱 상승되었다.

Doxorubicin에 의한 내인성 산화질소가 인간 대장암 세포주에서의 세포사멸에 미치는 효과 (Endogenous Nitric Oxide Strengthens Doxorubicin-induced Apoptosis in Human Colorectal Cell Lines)

  • 임순재;김지혜;김민영
    • 생명과학회지
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    • 제24권10호
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    • pp.1137-1143
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    • 2014
  • Doxorubicin은 광범위한 암을 치료하는데 사용되는 일반적인 항암제이지만, 내인성 산화질소 생성량과 Doxorubicin의 항암 효과의 상관 관계에 대해서는 아직 명확하게 밝혀지지 않았다. 본 연구에서는 인간 대장암 세포에서 Doxorubicin의 항암 활성에 내인성 산화질소가 미치는 영향을 확인하고자 하였다. HCT116 (p53-WT)과 HT29 (p53-MUT) 세포에서 Doxorubicin 처리에 의해 세포 생존율의 차이를 보였으며, NMA 병행처리는 Doxorubicin의 효과를 감소시켰음을 확인할 수 있었다. 추가 연구를 통해 HCT116과 HT29 세포에서 sub-$G_1$ 기의 세포 빈도와 DNA 단편화의 결과를 통해 내인성 산화질소가 Doxorubicin에 의한 apoptosis를 조절하는 것을 확인하였다. 이러한 결과는 인간 대장암 세포에서 내인성 산화질소와 IAP 발현, p53의 상태에 따른 조절이 Doxorubicin에 의해 유도된다는 것을 보여주며, 이러한 메커니즘은 대장암에서 화학요법의 효율을 향상시키기 위한 전략적인 표적으로 이용할 수 있을 것으로 생각된다.

Enhancement of Anti-tumorigenic Polysaccharide Production, Adhesion, and Branch Formation of Bifidobacterium bifidum BGN4 by Phytic Acid

  • Ku, Seock-Mo;You, Hyun-Ju;Ji, Geun-Eog
    • Food Science and Biotechnology
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    • 제18권3호
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    • pp.749-754
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    • 2009
  • The polysaccharide (BB-pol) extracted from Bifidobacterium bifidum BGN4 showed growth inhibitory effects on several colon cancer cell lines such as HT-29 and HCT-116. To increase the yield of polysaccharide, B. bifidum BGN4 was cultured in various culture media with different compositions. When B. bifidum BGN4 was cultured in modified MRS broth containing phytic acid, the cells showed increased branch formation and enlarged morphology. The content of total carbohydrate and the ability of adhesion to intestinal epithelial cells were also increased by phytic acid. The polysaccharide obtained from the cells grown in the presence of phytic acid inhibited the proliferation of cancer cell lines such as HT-29 and MCF-7 cells but not normal colon cell line, FHC. Taken together, Bifidobacterium grown in the presence of phytic acid may confer enhanced beneficial function for the host.

Activation of SAPK and Increase in Bak Levels during Ceramide and Indomethacin-Induced Apoptosis in HT29 Cells

  • Kim, Ju-Ho;Oh, Sae-Ock;Jun, Sung-Sook;Jung, Jin-Sup;Woo, Jae-Suk;Kim, Yong-Keun;Lee, Sang-Ho
    • The Korean Journal of Physiology and Pharmacology
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    • 제3권1호
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    • pp.75-82
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    • 1999
  • It has been reported that activation of sphingomyelin pathway and nonsteroidal anti-inflammatory drugs (NSAIDS) inhibit the promotion of colon carcinoma. Ceramide, a metabolite of sphingomyelin, and indomethacin were shown to induce apoptosis in colon carcinoma cells. However, the mechanisms of ceramide- and indomethacin-induced apoptosis in the colon carcinoma cells are not clearly elucidated. Recent studys showed that indomethacin-induced apoptosis in colon cancer cells through the cyclooxygenase-independent pathways, and that may be mediated by generation of ceramide. In this study, we compared effects of ceramide and indomethacin on important modulators of apoptotic processes in HT29 cells, a human colon cancer cell line. Ceramide and indomethacin induced apoptosis dose- and time- dependently. Ceramide and indomethacin increased stress-activated protein kinase (SAPK) activity, and decreased mitogen-activated protein kinase (MAPK) activity. The expression of Bak was increased by the treatment of ceramide and indomethacin. The expression of other Bcl-2 related proteins (Mcl-1, $Bcl-X_L,$ Bax) which were known to be expressed in colon epithelial cells was not changed during the ceramide- and indomethacin-induced apoptosis. Our results suggest that ceramide and indomethacin share common mechanisms for induction of apoptosis in HT29 cells.

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Antimutagenic and Anticancer Effects of Leaf Mustard and Leaf Mustard Kimchi

  • Kim, Yong-Taek;Kim, Boh-Kyung;Park, Kun-Young
    • Preventive Nutrition and Food Science
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    • 제12권2호
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    • pp.84-88
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    • 2007
  • In this study, we investigated antimutagenic and anticancer activities of leaf mustard (LM, Brassica juncea) and leaf mustard kimchi (LMK) during their fermentation period. Methanol extracts were prepared from raw mustard, brined leaf mustard in 10% Gueun salt solution for 2 hrs, leaf mustard fermented at 15$^{\circ}C$ for 5 days after brined in 10% Guenun salt solution for 2 hrs (Fr-LM), fresh leaf mustard kimchi (Fresh-LMK) and optimally ripened leaf mustard kimchi fermented at 5$^{\circ}C$ for 30 days (OR-LMK). OR-LMK showed the strongest inhibitory activities against the mutagenicities induced by aflatoxin B1 in Salmonella Typhimurium TA100. LMs and LMKs inhibited the survival or growth of AGS human gastric adenocarcinoma cells and HT-29 human colon carcinoma cells in MTT assay and growth inhibition test. Among the extracts, OR-LMK and FR-LM exhibited strong antiproliferative effect against cancer cells, especially HT-29 cells. DAPI staining assay showed that OR-LMK induced apoptosis cell death of HT-29 cells in a dose-dependent manner. These results suggest that leaf mustards and leaf mustard kimchi have chemopreventive activities.

곽향과 갈근 복합제제의 대장암 세포주 HT-29 증식 저해효과 및 $PGE_2$ 생성 억제효과 (Inhibitory Effect of Mixture of Ethanol Extracts in Agastachis Herba and Pueraria Radix on the Proliferation and $PGE_2$ Production of HT-29 Human Colon Cancer Cell Line)

  • 이승연;김희석;김정옥;황성완;황성연
    • 생약학회지
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    • 제37권4호
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    • pp.283-289
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    • 2006
  • Ethanol extracts of the whole herb of Agastachis Herba (A) and of Pueraria Radix (P) alone and of their mixture (A+P) downregulated the cell growth, cyclooxygenase-2 (COX-2) expression, prostaglandin $E_2\;(PGE_2)$, and cGMP production. A, P, and A + P inhibited the cell growth of HT-29 colon cancer cells in a concentration- and time-dependent manner but not the growth of normal colon cell, CCD-112CoN. In addition, they markedly inhibited the productions of $PGE_2$ and cGMP as well as the mRNA expression of COX-2. These data suggest that non-toxic concentration of A, P, and A + P have a significant effect on the in vitro growth of HT-29 cells, specifically through the inhibition of the $PGE_2$ production via COX-2.

고려인삼중 지용성 성분이 인체암 세포의 수종 효소활성에 미치는 영향. (Effects of Petroleum Ether Extract of Ginseng Root on Some Enzyme Activity in Human Colon Cancer Cells)

  • 황우익;오수경
    • Journal of Ginseng Research
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    • 제10권1호
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    • pp.27-35
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    • 1986
  • 본 연구는 인삼중 지용성 성분이 인체암 세포의 증식억제와 암세포내 효소 활성에 미치는 영향을 구명하고자 실시하였다. 인체 장암 세포인 HRT-18, HCT-48 및 HT-29등을 대상으로 인삼추출물 처리시 각 암세포의 증식율과 암세포내 효소 즉, sucrase, lactase, maltase 및 trehalase등 disaccharidas 활성을 측정한 바 다음과 같은 결과를 얻었다. 1. HTR-18, HT-29 및 HCT-48의 doubling time은 각각 약 20, 22, 24시간이 및 되었다. 2. 각 암세포의 증식율은 배양액 중 CX 함량의 증가와 연장에 따라 점차 더 억제되었다. 3. 인삼 extract를 함유하는 배양액에서 배양된 HRT-18 및 HCT-48 암세포의 sucarse활성은 각각 362% 및 577% 증가하였고, lactase(317%, 334%), maltase(134% 및 153%) 및 trehalase(311% 및 203%) 활성도 다 같이 유의성있게 증가하였다.

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Combination of Nimbolide and TNF-α-Increases Human Colon Adenocarcinoma Cell Death through JNK-mediated DR5 Up-regulation

  • Boonyarat, Chantana;Yenjai, Chavi;Reubroycharoen, Prasert;Waiwut, Pornthip
    • Asian Pacific Journal of Cancer Prevention
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    • 제17권5호
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    • pp.2637-2641
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    • 2016
  • Tumor necrosis factor ($TNF-{\alpha}$), an inflammatory cytokine that plays an important role in the control of cell proliferation, differentiation, and apoptosis, has previously been used in anti-cancer therapy. However, the therapeutic applications of $TNF-{\alpha}$ are largely limited due to its general toxicity and anti-apoptotic influence. To overcome this problem, the present study focused on the effect of active constituents isolated from a medicinal plant on $TNF-{\alpha}$-induced apoptosis in human colon adenocarcinoma (HT-29) cells. Nimbolide from Azadirachta indica was evaluated for cytotoxicity by methyl tetrazolium 3-[4,5-dimethylthiazol-2-yl]-2, 5-diphenyltetrazolium bromide (MTT) assay and phase contrast microscopy. Effects on apoptotic signaling proteins were investigated using Western blot analysis. Nimbolide showed cytotoxicity against HT-29 cells that was significantly different from the control group (p<0.01), a concentration of $10{\mu}M$ significantly inducing cell death (p<0.01). In combination with $TNF-{\alpha}$, nimbolide significantly enhanced-induced cell death. In apoptotic pathway, nimbolide activated c-Jun N-terminal kinase (JNK) phosphorylation, BH3 interacting-domain death agonist (Bid) and up-regulated the death receptor 5 (DR5) level. In the combination group, nimbolide markedly sensitized $TNF-{\alpha}$-induced JNK, Bid, caspase-3 activation and the up-regulation of DR5. Our findings overall indicate that nimbolide may enhance $TNF-{\alpha}$-mediated cellular proliferation inhibition through increasing cell apoptosis of HT-29 cells by up-reglation of DR5 expression via the JNK pathway.

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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    • 제15권23호
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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.

CoMSIA 3D-QSAR Analysis of 3,4-Dihydroquinazoline Derivatives Against Human Colon Cancer HT-29 Cells

  • Kwon, Gi Hyun;Cho, Sehyeon;Lee, Jinsung;Sohn, Joo Mi;Byun, Joon Seok;Lee, Kyung-Tae;Lee, Jae Yeol
    • Bulletin of the Korean Chemical Society
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    • 제35권11호
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    • pp.3181-3187
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    • 2014
  • A series of 3,4-dihydroquinazoline derivatives with anti-cancer activities against human colon cancer HT-29 cell were subjected to three-dimensional quantitative structure-activity relationship (3D-QSAR) studies using the comparative molecular similarity indices analysis (CoMSIA) approaches. The most potent compound, BK10001 was used to align the molecules. As a result, the best prediction was obtained with CoMSIA combined electrostatic, hydrophobic, and hydrogen-bond acceptor fields ($q^2=0.648$, $r^2=0.882$). This model was validated by an external test set of six compounds giving satisfactory predictive $r^2$ values of 0.879. This model would guide the design of potent 3,4-dihydroquinazoline derivatives as anti-cancer agent for the treatment of human colon cancer.