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Träfflista för sökning "WFRF:(Wiman B) srt2:(2000-2004)"

Sökning: WFRF:(Wiman B) > (2000-2004)

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  • Bruun-Lundgren, Maria, 1949, et al. (författare)
  • Industrial activities and personal adornments
  • 2000
  • Ingår i: The Greek-Swedish excavations at the Agia Aikaterini Square, Kastelli, Khania 1970-1987 : results of the excavations under the direction of Yannis Tzedakis and Carl-Gustaf Styrenius. Vol. 2, The Late Minoan IIIC settlement : text and plates. - 9179160417 ; 2, s. 175-183
  • Bokkapitel (övrigt vetenskapligt/konstnärligt)
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  • Girnita, L., et al. (författare)
  • Increased expression of insulin-like growth factor I receptor in malignant cells expressing aberrant p53 : Functional impact
  • 2000
  • Ingår i: Cancer Research. - 0008-5472 .- 1538-7445. ; 60:18, s. 5278-5283
  • Tidskriftsartikel (refereegranskat)abstract
    • 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.
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