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Enhanced expression of cyclooxygenase-2 and nuclear beta-catenin are related to mutations in the APC gene in human colorectal cancer

Dimberg, Jan, (författare)
Linköpings universitet, Cellbiologi, Linköpings universitet, Hälsouniversitetet
Hugander, A, (författare)
Univ Jonkoping, Coll Hlth Sci, Dept Nat Sci & Biomed, S-55111 Jonkoping, Sweden Fac Hlth Sci, Div Cell Biol, Dept Biomed & Surg, Linkoping, Sweden Ryhov Cty Hosp, Dept Surg, Jonkoping, Sweden Karolinska Hosp, Karolinska Inst, Ctr Mol Med, S-10401 Stockholm, Sweden
Sirsjo, A, (författare)
Univ Jonkoping, Coll Hlth Sci, Dept Nat Sci & Biomed, S-55111 Jonkoping, Sweden Fac Hlth Sci, Div Cell Biol, Dept Biomed & Surg, Linkoping, Sweden Ryhov Cty Hosp, Dept Surg, Jonkoping, Sweden Karolinska Hosp, Karolinska Inst, Ctr Mol Med, S-10401 Stockholm, Sweden
visa fler...
Söderkvist, Peter, (författare)
Linköpings universitet, Hälsouniversitetet, Linköpings universitet, Cellbiologi
visa färre...
2001
Engelska.
Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 21:2A, s. 911-915
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
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  • <p>Mutational inactivation of the human tumour suppressor gene adenomatous polyposis coli (APC) results in constitutive activation of beta -catenin/T cell factor-4 (Tcf-4) mediated transcription of target genes. Up-regulation of cyclooxygenase-2 (COX-2) protein is frequently found in human colorectal cancer (CRC). We analysed 38 CRC for mutations in APC and beta -catenin and found an association between APC mutations and elevated COX-2 levels. Furthermore, APC mutations were predominantly observed in tumour tissues from the rectum compared to tumours of colonic origin. Western blot analysis revealed that nuclear beta -catenin levels were generally higher in tumours with APC mutations compared to tumours with wild type APC. However, there was also a higher level of nuclear beta -catenin in tumour compared to normal tissue, hut nuclear Tcf-4 protein was constitutively expressed in tumour and normal tissue and showed no differences. An identified putative Tcf-4 binding element in the COX-2 promoter may partly explain the enhanced level of COX-2 and support the idea that COX-2 may be a downstream target of the APC/beta -catenin/Tcf-4 pathway.</p>

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  (hsv//swe)
MEDICAL AND HEALTH SCIENCES  (hsv//eng)

Nyckelord

cyclooxygenase-2
beta-catenin
Tcf-4
APC
colorectal cancer
MEDICINE
MEDICIN

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