SwePub
Sök i LIBRIS databas

  Extended search

onr:"swepub:oai:DiVA.org:kth-20056"
 

Search: onr:"swepub:oai:DiVA.org:kth-20056" > Increased expressio...

  • 1 of 1
  • Previous record
  • Next record
  •    To hitlist
  • Girnita, L.Karolinska Institutet (author)

Increased expression of insulin-like growth factor I receptor in malignant cells expressing aberrant p53 : Functional impact

  • Article/chapterEnglish2000

Publisher, publication year, extent ...

  • 2000
  • printrdacarrier

Numbers

  • LIBRIS-ID:oai:DiVA.org:kth-20056
  • https://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-20056URI
  • http://kipublications.ki.se/Default.aspx?queryparsed=id:1931520URI

Supplementary language notes

  • Language:English
  • Summary in:English

Part of subdatabase

Classification

  • Subject category:ref swepub-contenttype
  • Subject category:art swepub-publicationtype

Notes

  • QC 20100525
  • We investigated the functional impact of p53 on insulin-like growth factor I receptor (IGF-IR) expression in malignant cells. Using the BL-41tsp53-2 cell line, a transfectant carrying temperature-sensitive (ts) p53 and endogenous mutant p53 (codon 248), we demonstrated a drastic down-regulation of plasma membrane-bound IGF-IRs on induction of wild-type p53, However, a similar response was obtained by treatment of BL-41tsp53-2 cells expressing mutant ts p53 with a p53 antisense oligonucleotide. Thus, even if the negative effect of wild-type p53 predominates under a competitive condition, these data indicate that mutant p53 may be important for up-regulation of IGF-IR, To further elucidate this issue, three melanoma cell lines (BE, SK-MEL-5, and SK-MEL-28) that over expressed p53 were investigated. The BE cell line has a hot spot mutation (codon 248) and expresses only codon 248-mutant p53, SK-MEL-28 has a point mutation at codon 145. SK-MEL-5 cells did not exhibit any p53 mutations, but the absence of p21(Waf1) expression suggested functionally aberrant p53. Our data suggest that interaction with Mdm-2 may underlie p53 inactivation in these cells, Using p53 antisense oligonucleotides, we demonstrated a substantial down-regulation of cell surface expression of IGF-IR proteins in all melanoma cell lines after 24 h, This was paralleled by decreased tyrosine phosphorylation of IGF-IR and growth arrest, and, subsequently, massive cell death was observed (this was also seen in BL-41tsp53-2 cells with mutant conformation of ts p53). Taken together, our results suggest that up-regulation of IGF-IR as a result of expression of aberrant p53 may be important for the growth and survival of malignant cells.

Subject headings and genre

  • human-melanoma cells
  • n-linked glycosylation
  • mutant p53
  • wild-type
  • inhibition
  • gene
  • apoptosis
  • mutation
  • lines
  • mechanisms

Added entries (persons, corporate bodies, meetings, titles ...)

  • Girnita, A.Karolinska Institutet (author)
  • Brodin, B.Karolinska Institutet (author)
  • Xie, Y. T. (author)
  • Nilsson, G.Karolinska Institutet (author)
  • Dricu, A. (author)
  • Lundeberg, JoakimKTH,Bioteknologi(Swepub:kth)u1qkn9kw (author)
  • Wejde, J.Karolinska Institutet (author)
  • Bartolazzi, A.Karolinska Institutet (author)
  • Wiman, K. G.Karolinska Institutet (author)
  • Larsson, O.Karolinska Institutet (author)
  • Karolinska InstitutetBioteknologi (creator_code:org_t)

Related titles

  • In:Cancer Research60:18, s. 5278-52830008-54721538-7445

Internet link

Find in a library

To the university's database

  • 1 of 1
  • Previous record
  • Next record
  •    To hitlist

Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.

 
pil uppåt Close

Copy and save the link in order to return to this view