1-25(oh)2-16-ene-23-yne-26-27-hexafluoro-19-nor-d3 and Colonic-Neoplasms

1-25(oh)2-16-ene-23-yne-26-27-hexafluoro-19-nor-d3 has been researched along with Colonic-Neoplasms* in 1 studies

Other Studies

1 other study(ies) available for 1-25(oh)2-16-ene-23-yne-26-27-hexafluoro-19-nor-d3 and Colonic-Neoplasms

Article	Year
A vitamin D analogue inhibits colonic carcinogenesis in the AOM/DSS model. The Journal of surgical research, 2007, Volume: 142, Issue:2 The azoxymethane (AOM) model recapitulates many features of human colon cancer, lacking an inflammatory component. Dextran sulfate sodium (DSS) induces colitis and promotes AOM-induced colon cancer in mice. Vitamin D analogues are anti-inflammatory and chemopreventive in models of colon cancer. Our aim was to evaluate the anti-inflammatory and chemopreventive efficacy of the vitamin D analogue Ro26-2198 in the AOM/DSS model and in vitro in HCA-7 colon cancer cells.. A/J mice received Ro26-2198 (0.01 microg/kg body wt/day x 28 days) or vehicle by mini-osmotic pump. Animals were treated with a single dose of AOM (5 mg/kg body wt) or vehicle 1 week after pump insertion. Mice received 3% DSS or water x 7 days beginning week 3. Animals were sacrificed after 8 weeks and colon segments were fixed in formalin or flash-frozen. Hematoxylin and eosin colonic sections were examined for dysplasia and colonic lysates were assessed for c-Myc, cyclooxygenase 2, and phospho-(active) extracellular signal regulated kinase (ERK) by Western blotting. For in vitro studies, HCA-7 cells were treated with Ro26-2198 followed by interleukin-1beta (IL-1beta). Proliferation was measured by WST-1 assay.. Ro26-2198 delayed the onset of clinical colitis. Several dysplastic foci were present in the AOM/DSS group; none were found in the Ro26-2198 group. Compared with control, AOM/DSS significantly increased c-Myc (15-fold), cyclooxygenase 2 (COX-2) (2.5-fold), and pERK (10-fold), and Ro26-2198 abolished these increases. In vitro, Ro26-2198 inhibited IL-1beta-induced ERK activation and COX-2 induction and decreased HCA-7 cell proliferation.. Ro26-2198 inhibited proliferative (ERK, c-Myc) and pro-inflammatory (COX-2) signals and progression to dysplasia, suggesting chemopreventive efficacy in this model of colitis-associated carcinogenesis. Topics: Adenocarcinoma; Animals; Anti-Inflammatory Agents; Cell Division; Cell Line, Tumor; Cholecalciferol; Colitis; Colon; Colonic Neoplasms; Cyclooxygenase 2; Disease Models, Animal; Extracellular Signal-Regulated MAP Kinases; Humans; Interleukin-1beta; Male; MAP Kinase Signaling System; Mice; Mice, Inbred A; Proto-Oncogene Proteins c-myc; Up-Regulation	2007

Article

Year

A vitamin D analogue inhibits colonic carcinogenesis in the AOM/DSS model.

The Journal of surgical research, 2007, Volume: 142, Issue:2

The azoxymethane (AOM) model recapitulates many features of human colon cancer, lacking an inflammatory component. Dextran sulfate sodium (DSS) induces colitis and promotes AOM-induced colon cancer in mice. Vitamin D analogues are anti-inflammatory and chemopreventive in models of colon cancer. Our aim was to evaluate the anti-inflammatory and chemopreventive efficacy of the vitamin D analogue Ro26-2198 in the AOM/DSS model and in vitro in HCA-7 colon cancer cells.. A/J mice received Ro26-2198 (0.01 microg/kg body wt/day x 28 days) or vehicle by mini-osmotic pump. Animals were treated with a single dose of AOM (5 mg/kg body wt) or vehicle 1 week after pump insertion. Mice received 3% DSS or water x 7 days beginning week 3. Animals were sacrificed after 8 weeks and colon segments were fixed in formalin or flash-frozen. Hematoxylin and eosin colonic sections were examined for dysplasia and colonic lysates were assessed for c-Myc, cyclooxygenase 2, and phospho-(active) extracellular signal regulated kinase (ERK) by Western blotting. For in vitro studies, HCA-7 cells were treated with Ro26-2198 followed by interleukin-1beta (IL-1beta). Proliferation was measured by WST-1 assay.. Ro26-2198 delayed the onset of clinical colitis. Several dysplastic foci were present in the AOM/DSS group; none were found in the Ro26-2198 group. Compared with control, AOM/DSS significantly increased c-Myc (15-fold), cyclooxygenase 2 (COX-2) (2.5-fold), and pERK (10-fold), and Ro26-2198 abolished these increases. In vitro, Ro26-2198 inhibited IL-1beta-induced ERK activation and COX-2 induction and decreased HCA-7 cell proliferation.. Ro26-2198 inhibited proliferative (ERK, c-Myc) and pro-inflammatory (COX-2) signals and progression to dysplasia, suggesting chemopreventive efficacy in this model of colitis-associated carcinogenesis.

Topics: Adenocarcinoma; Animals; Anti-Inflammatory Agents; Cell Division; Cell Line, Tumor; Cholecalciferol; Colitis; Colon; Colonic Neoplasms; Cyclooxygenase 2; Disease Models, Animal; Extracellular Signal-Regulated MAP Kinases; Humans; Interleukin-1beta; Male; MAP Kinase Signaling System; Mice; Mice, Inbred A; Proto-Oncogene Proteins c-myc; Up-Regulation

2007