RGD Reference Report - Angiostatic properties of sulindac and celecoxib in the experimentally induced inflammatory colorectal cancer. - Rat Genome Database

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Angiostatic properties of sulindac and celecoxib in the experimentally induced inflammatory colorectal cancer.

Authors: Vaish, V  Piplani, H  Rana, C  Sanyal, SN 
Citation: Vaish V, etal., Cell Biochem Biophys. 2013 Jun;66(2):205-27. doi: 10.1007/s12013-012-9469-4.
RGD ID: 8657112
Pubmed: PMID:23149858   (View Abstract at PubMed)
DOI: DOI:10.1007/s12013-012-9469-4   (Journal Full-text)

Initiation of various cancers has been observed to be regulated via a prolonged inflammatory state in the tissues. However, molecular role of such a localized inflammation is not clear in the advanced stages of colorectal cancer. In this study, we have elaborated the role of various pro- and anti-inflammatory cytokines, transcription, and angiogenic factors in the progression of the 1,2-dimethylhydrazine dihydrochloride (DMH)-induced late phage colorectal cancer and also observed the chemopreventive role of the two non-steroidal anti-inflammatory drugs (NSAIDs), viz., Sulindac and Celecoxib. Carcinogenic changes were observed with morphological and histopathological studies, whereas mRNA and protein regulations of various biomolecules were identified via RT- or qRT-PCR, western blot and immunofluorescence analysis, respectively. Activity of inducible nitric oxide (NO) and cyclooxygenase-2 enzymes were analyzed using standard NO assay and prostaglandin E2 immunoassay, whereas activities of matrix metalloproteinases (MMP-2 and-9) were identified by gelatin zymography. Flowcytometry was performed for the relative quantification of the apoptotic events. Molecular docking studies of Sulindac and Celecoxib were also performed with different target proteins to observe their putative mechanisms of action. As a result, we found that DMH-treated animals were having over-expression of various pro-inflammatory cytokines (IL-1beta, IL-2, and IFNgamma), aberrant nuclear localization of activated cell survival transcription factors (NF-kappaB and Stat3) along with the increased incidence of activated angiogenic factors (MMP-2 and MMP-9) suggesting a marked role of inflammation in the tumor progression. However, NSAIDs co-administration has significantly reduced the angiogenic potential of the growing neoplasm.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Colorectal Neoplasms treatmentISOMmp2 (Rattus norvegicus)8657112; 8657112 RGD 
Colorectal Neoplasms treatmentISOMmp9 (Rattus norvegicus)8657112; 8657112 RGD 
Colorectal Neoplasms treatmentIEP 8657112; 8657112 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Mmp2  (matrix metallopeptidase 2)
Mmp9  (matrix metallopeptidase 9)

Genes (Mus musculus)
Mmp2  (matrix metallopeptidase 2)
Mmp9  (matrix metallopeptidase 9)

Genes (Homo sapiens)
MMP2  (matrix metallopeptidase 2)
MMP9  (matrix metallopeptidase 9)


Additional Information