scholarly journals Hormonal control of fructose 2,6-bisphosphate concentration in the HT29 human colon adenocarcinoma cell line α2-adrenergic agonists counteract effect of vasoactive intestinal peptide

1986 ◽  
Vol 239 (3) ◽  
pp. 531-536 ◽  
Author(s):  
C Denis ◽  
H Paris ◽  
J C Murat
Keyword(s):  
Cyclic Amp ◽  
Cancer Cells ◽  
Vasoactive Intestinal Peptide ◽  
Colon Adenocarcinoma ◽  
Human Colon ◽  
Hormonal Control ◽  
Maximum Effect ◽  
Dose Dependent Decrease ◽  
Dose Dependent ◽  
Human Colon Adenocarcinoma

Vasoactive intestinal peptide (VIP) was found to cause a dose-dependent decrease in fructose 2,6-bisphosphatase concomitant with an increase in cyclic AMP in cultured HT29 cancer cells from human colon. The maximum effect was a 41% decrease obtained with 10 nM-VIP, and half-maximum effect was obtained with 0.75 nM-VIP. The effect of 2.5 nM-VIP was almost totally counteracted (i.e. fructose 2,6-bisphosphate concentration was restored) by either adrenaline (1 microM) or the alpha 2-adrenergic agonist UK-14304 (1 microM); the alpha 2-agonist clonidine (1 microM) was less efficient, since the VIP effect was decreased by 72% only. The adrenaline effect was totally antagonized by 1 microM-yohimbine. It is concluded that, in the HT29 cancer cells, the fructose 2,6-bisphosphate-producing system is sensitive to variations of cyclic AMP concentration and is under the dual control of VIP and alpha 2-adrenergic receptors.

scholarly journals Cytotoxic Effects of Four Aescin Types on Human Colon Adenocarcinoma Cell Lines

2014 ◽  
Vol 9 (3) ◽  
pp. 1934578X1400900 ◽  
Author(s):  
Ewa Seweryn ◽  
Michał Glehsk ◽  
Kamila Środa-Pomianek ◽  
Ireneusz Ceremuga ◽  
Maciej Włodarczyk ◽  
...  
Keyword(s):  
Cell Lines ◽  
Colon Adenocarcinoma ◽  
Human Colon ◽  
Cytotoxic Activities ◽  
Cytotoxic Effects ◽  
Adenocarcinoma Cell ◽  
Sulforhodamine B ◽  
Dose Dependent ◽  
Mtt Assays ◽  
Human Colon Adenocarcinoma

Four types of aescin that are available on the pharmaceutical market, β-aescin crystalline, β-aescin amorphous, β-aescin sodium and aescin polysulfate, have been analyzed for their cytotoxic effects on human colon adenocarcinoma (LoVo) and doxorubicin-resistant human colon adenocarcinoma cell lines (LoVo/Dx). Their cytotoxic activities were evaluated by sulforhodamine B (SRB) and methyl tetrazolium (MTT) assays. All four types of aescin exerted strong dose-dependent cytotoxicity to LoVo and, to a lesser degree, LoVo/Dx cell lines. The IC50 value for the LoVo/Dx cell line was higher, but still dose-dependent. Results from both assays demonstrated that β-aescin crystalline has the most cytotoxic activity toward human colon adenocarcinoma cell lines.

Vasoactive intestinal peptide and forskolin regulate proliferation of the HT29 human colon adenocarcinoma cell line

1992 ◽  
Vol 150 (3) ◽  
pp. 501-509 ◽  
Author(s):  
Laurence Gamet ◽  
Jean-Claude Murat ◽  
Anne Remaury ◽  
Christian Remesy ◽  
Philippe Valet ◽  
...  
Keyword(s):  
Cell Line ◽  
Vasoactive Intestinal Peptide ◽  
Colon Adenocarcinoma ◽  
Human Colon ◽  
Adenocarcinoma Cell Line ◽  
Adenocarcinoma Cell ◽  
Human Colon Adenocarcinoma

scholarly journals Molecular identification and structural requirement of vasoactive intestinal peptide (VIP) receptors in the human colon adenocarcinoma cell line, HT-29

1985 ◽  
Vol 231 (1) ◽  
pp. 139-143 ◽  
Author(s):  
A Couvineau ◽  
M Rousset ◽  
M Laburthe
Keyword(s):  
Cell Line ◽  
Vasoactive Intestinal Peptide ◽  
Colon Adenocarcinoma ◽  
Human Colon ◽  
Adenocarcinoma Cell Line ◽  
Structural Requirement ◽  
Adenocarcinoma Cell ◽  
Ht 29 ◽  
Human Colon Adenocarcinoma ◽  
Vip Receptor

The human colon adenocarcinoma cell line HT-29 in culture exhibits a cyclic AMP production system highly sensitive to vasoactive intestinal peptide (VIP), making HT-29 cells a unique cultured cell system for studying the mechanism of VIP action [Laburthe, Rousset, Boissard, Chevalier, Zweibaum & Rosselin (1978) Proc. Natl. Acad. Sci. U.S.A. 75, 2772-2775]. The quantitative characteristics of VIP receptors in HT-29 cells and their structural requirement and molecular size were studied. 125I-labeled VIP bound in a time-dependent manner to HT-29 cell homogenates. At equilibrium (60 min incubation at 30 degrees C), unlabelled VIP in the 0.01-10 nM concentration range competed with 125I-VIP for binding to cell homogenates. Scatchard analysis of binding data gave a straight line, indicating that VIP bound to a single population of sites with a KD of 0.12 +/- 0.02 nM and a capacity of 120 +/- 9 fmol/mg of protein. The structural requirement of these receptors was studied with peptides structurally related to VIP, either natural or synthetic. Several peptides inhibited 125I-VIP binding to HT-29 cell homogenates with the following order of potency, which is typical of the human VIP receptor: VIP (IC50 = 0.1 nM) greater than VIP-(2-28)-peptide (IC50 = 13 nM) greater than human growth hormone releasing factor (IC50 = 56 nM) greater than peptide histidine isoleucine amide (IC50 = 80 nM) greater than secretin (IC50 greater than 10 000 nM). To characterize the molecular component(s) of the VIP receptor in HT-29 cells, 125I-VIP was covalently bound to cell homogenates by using the cross-linker dithiobis(succinimidyl propionate). Sodium dodecyl sulphate/polyacrylamide-gel autoradiographic studies of affinity-labelled cell homogenates revealed two major bands, corresponding to 125I-VIP-protein complexes of Mr 66 000 and 16 000. The labelling of the Mr-66 000 component was specific, since it was abolished by native VIP, whereas that of the Mr-16 000 component was not. Densitometric scanning of autoradiographs indicated that the labelling of the Mr-66 000 complex was inhibited by low VIP concentrations in the 0.1-10 nM range (IC50 = 0.6 nM), but was unaffected by 1 microM-glucagon or octapeptide of cholecystokinin. It was also decreased by VIP-(2-28)-peptide with a potency 1% that of VIP. Assuming that one molecule of 125I-VIP bound per molecule of protein, one protein of Mr 63 000 was identified as a component of the VIP receptor in HT-29 cells.

scholarly journals Pyruvate Treatment Restores the Effectiveness of Chemotherapeutic Agents in Human Colon Adenocarcinoma and Pleural Mesothelioma Cells

2018 ◽  
Vol 19 (11) ◽  
pp. 3550 ◽  
Author(s):  
Eleonora Mungo ◽  
Loredana Bergandi ◽  
Iris Salaroglio ◽  
Sophie Doublier
Keyword(s):  
Multidrug Resistance ◽  
Cancer Cells ◽  
Colon Adenocarcinoma ◽  
Glucose Consumption ◽  
Mitochondrial Respiratory Chain ◽  
Human Colon ◽  
Chemotherapeutic Agents ◽  
Cross Resistance ◽  
Ht29 Cells ◽  
Human Colon Adenocarcinoma

Emerging evidence supports the idea that a dysfunction in cell metabolism could sustain a resistant phenotype in cancer cells. As the success of chemotherapeutic agents is often questioned by the occurrence of multidrug resistance (MDR), a multiple cross-resistance towards different anti-cancer drugs represent a major obstacle to cancer treatment. The present study has clarified the involvement of the carbon metabolites in a more aggressive tumor colon adenocarcinoma phenotype and in a chemoresistant mesothelioma, and the role of pyruvate treatment in the reversion of the potentially related resistance. For the first time, we have shown that human colon adenocarcinoma cells (HT29) and its chemoresistant counterpart (HT29-dx) displayed different carbon metabolism: HT29-dx cells had a higher glucose consumption compared to HT29 cells, whereas human malignant mesothelioma (HMM) cells showed a lower glucose consumption compared to HT29 cells, accompanied by a lower pyruvate production and, consequently, a higher production of lactate. When treated with pyruvate, both HT29-dx and HMM cells exhibited a re-established accumulation of doxorubicin and a lower survival ability, a decreased activity of multidrug resistance protein 1 (MRP1) and a restored mitochondrial respiratory chain function, improving the effectiveness of the chemotherapeutic agents in these resistant cancer cells.

scholarly journals STAT6 mRNA and protein knockdown using multiple siRNA sequences inhibits proliferation and induces apoptosis of the human colon adenocarcinoma cell line, HT-29

2018 ◽  
Author(s):  
C. Salguero-Aranda ◽  
D. Sancho-Mensat ◽  
S. Sultan ◽  
A. Reginald ◽  
L. Chapman
Keyword(s):  
Cancer Cells ◽  
Colon Adenocarcinoma ◽  
Human Colon ◽  
Colorectal Cancers ◽  
Colon Cancer Cells ◽  
Adenocarcinoma Cell Line ◽  
Adenocarcinoma Cell ◽  
Individual Sequences ◽  
Ht 29 ◽  
Human Colon Adenocarcinoma

AbstractThe transcription factor STAT6 is strongly expressed in various tumours and is most highly expressed in malignant lymphomas and pancreatic, colorectal, prostate and breast cancers. STAT6 expression in colorectal cancer is associated with an increased malignancy, poor prognosis and poor survival rates. Colorectal cancer has an incidence of approximately 1,361,000 patients per annum worldwide and approximately 60% of those cancers show STAT6 expression. Techniques aimed at reducing or blocking STAT6 expression may be useful in treating colorectal cancers. Celixir’s four proprietary STAT6 specific small interfering RNA (siRNA) sequences were tested in vitro using the human colon adenocarcinoma cell line, HT-29. The four sequences were introduced individually and in combination into HT-29 cells at different concentrations (10 to 200 nM). Decreases in STAT6 mRNA and protein levels were analysed to confirm the transfection was successful. STAT6 knockdown effects were measured by analysing cell proliferation and apoptosis. Results showed that 100nM siRNA concentration was the most effective and all four individual sequences knocked-down STAT6 mRNA and protein by more than 50%. Although all individual sequences were capable of significantly inhibiting cell proliferation, STAT6.1 and STAT6.4 were the best. STAT6 silencing also significantly induced late and total apoptotic events. In conclusion, these results demonstrate that STAT6 siRNA sequences are capable of inhibiting the proliferation, and inducing late apoptosis, of HT-29 colon cancer cells and, in some instances, halving the number of cancer cells. These experiments will be repeated using xenografts of STAT6-expressing colon cancer cells in immunocompromised mice and the STAT6 siRNA sequences will be tested in other cancers in which STAT6 is expressed. The STAT6 siRNA sequences therefore represent a potential treatment for the most serious colorectal cancers and a wide variety of STAT6-expressing cancers.

scholarly journals The antioxidant potential of peptides obtained from the spotted babylon snail (Babylonia areolata) in treating human colon adenocarcinoma (Caco-2) cells

RSC Advances ◽  
2020 ◽  
Vol 10 (43) ◽  
pp. 25746-25757 ◽  
Author(s):  
Putcha Petsantad ◽  
Papassara Sangtanoo ◽  
Piroonporn Srimongkol ◽  
Tanatorn Saisavoey ◽  
Onrapak Reamtong ◽  
...  
Keyword(s):  
Antioxidant Activity ◽  
Cell Line ◽  
Synthetic Peptides ◽  
Colon Adenocarcinoma ◽  
Human Colon ◽  
Antioxidant Peptides ◽  
Babylonia Areolata ◽  
Dose Dependent ◽  
Human Colon Adenocarcinoma ◽  
Subsequent Identification

The isolation and subsequent identification of the two novel antioxidant peptides, HTYHEVTKH, and WPVLAYHF from the spotted babylon snail was achieved. In the Caco-2 cell line, two synthetic peptides produced a dose-dependent response on antioxidant activity.

scholarly journals A Link between FXYD3 (Mat-8)-mediated Na,K-ATPase Regulation and Differentiation of Caco-2 Intestinal Epithelial Cells

2009 ◽  
Vol 20 (4) ◽  
pp. 1132-1140 ◽  
Author(s):  
Stéphanie Bibert ◽  
David Aebischer ◽  
Florian Desgranges ◽  
Sophie Roy ◽  
Danièle Schaer ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Cancer Cells ◽  
Colon Adenocarcinoma ◽  
Human Colon ◽  
Intestinal Epithelial ◽  
Differentiation Markers ◽  
Adenocarcinoma Cells ◽  
Human Colon Adenocarcinoma ◽  
Colon Adenocarcinoma Cells

FXYD3 (Mat-8) proteins are regulators of Na,K-ATPase. In normal tissue, FXYD3 is mainly expressed in stomach and colon, but it is also overexpressed in cancer cells, suggesting a role in tumorogenesis. We show that FXYD3 silencing has no effect on cell proliferation but promotes cell apoptosis and prevents cell differentiation of human colon adenocarcinoma cells (Caco-2), which is reflected by a reduction in alkaline phosphatase and villin expression, a change in several other differentiation markers, and a decrease in transepithelial resistance. Inhibition of cell differentiation in FXYD3-deficient cells is accompanied by an increase in the apparent Na+ and K+ affinities of Na,K-ATPase, reflecting the absence of Na,K-pump regulation by FXYD3. In addition, we observe a decrease in the maximal Na,K-ATPase activity due to a decrease in its turnover number, which correlates with a change in Na,K-ATPase isozyme expression that is characteristic of cancer cells. Overall, our results suggest an important role of FXYD3 in cell differentiation of Caco-2 cells. One possibility is that FXYD3 silencing prevents proper regulation of Na,K-ATPase, which leads to perturbation of cellular Na+ and K+ homeostasis and changes in the expression of Na,K-ATPase isozymes, whose functional properties are incompatible with Caco-2 cell differentiation.

In Vitro and in Vivo Comparison of Binding of 99m-Tc-Iabeled Anti-CEA MAb F33-104 with 99m-Tc-labeled Anti-CEA MAb BW431/26

1999 ◽  
Vol 38 (04) ◽  
pp. 115-119
Author(s):  
N. Oriuchi ◽  
S. Sugiyama ◽  
M. Kuroki ◽  
Y. Matsuoka ◽  
S. Tanada ◽  
...  
Keyword(s):  
Nude Mice ◽  
Binding Capacity ◽  
Colon Adenocarcinoma ◽  
Human Colon ◽  
Cell Binding ◽  
Vitro Binding ◽  
Labeling Method ◽  
Human Colon Adenocarcinoma

Summary Aim: The purpose of this study was to assess the potential for radioimmunodetection (RAID) of murine anti-carcinoembryonic antigen (CEA) monoclonal antibody (MAb) F33-104 labeled with technetium-99m (99m-Tc) by a reduction-mediated labeling method. Methods: The binding capacity of 99m-Tc-labeled anti-CEA MAb F33-104 with CEA by means of in vitro procedures such as immunoradiometric assay and cell binding assay and the biodistribution of 99m-Tc-labeled anti-CEA MAb F33-104 in normal nude mice and nude mice bearing human colon adenocarcinoma LS180 tumor were investigated and compared with 99m-Tc-labeled anti-CEA MAb BW431/26. Results: The in vitro binding rate of 99m-Tc-labeled anti-CEA MAb F33-104 with CEA in solution and attached to the cell membrane was significantly higher than 99m-Tclabeled anti-CEA MAb BW431/261 (31.4 ± 0.95% vs. 11.9 ± 0.55% at 100 ng/mL of soluble CEA, 83.5 ± 2.84% vs. 54.0 ± 2.54% at 107 of LS 180 cells). In vivo, accumulation of 99m-Tc-labeled anti-CEA MAb F33-104 was higher at 18 h postinjection than 99m-Tc-labeled anti-CEA MAb BW431/26 (20.1 ± 3.50% ID/g vs. 14.4 ± 3.30% ID/g). 99m-Tcactivity in the kidneys of nude mice bearing tumor was higher at 18 h postinjection than at 3 h (12.8 ± 2.10% ID/g vs. 8.01 ± 2.40% ID/g of 99m-Tc-labeled anti-CEA MAb F33-104, 10.7 ± 1.70% ID/g vs. 8.10 ± 1.75% ID/g of 99m-Tc-labeled anti-CEA MAb BW431/26). Conclusion: 99m-Tc-labeled anti-CEA MAb F33-104 is a potential novel agent for RAID of recurrent colorectal cancer.

Sign in / Sign up

Export Citation Format

Share Document