Complex regulation of prothymosin alpha in mammary tumors arising arising in transgenic mice

Life Sci. 1999;64(23):2125-33. doi: 10.1016/s0024-3205(99)00161-7.

Abstract

Expression of prothymosin alpha (PTA) has been related to cell proliferation, both normal and pathological. PTA has also been proposed to be a target of the c-myc protooncogene. To study PTA mRNA levels during pathological cell growth, and especially the effect of the activation of specific oncogenes on PTA expression, we have studied its expression in tumors that arise in transgenic mice. We found high PTA levels in mammary tumors arising in c-myc, c-neu, and v-ras transgenic mice. Levels of this protein were variable between different tumors, and there is a differential regulation of PTA respect to other putative c-myc target genes, such as Ornithine Decarboxylase (ODC). Furthermore, expression of PTA is not absolutely dependent of c-myc expression, as shown by MYC depletion experiments performed with antisense oligonucleotides. We conclude that regulation of PTA in these tumors is complex and depends on more than a single activated oncogene.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cyclin B / genetics
  • Cyclin D1 / genetics
  • Cyclin E / genetics
  • Female
  • Gene Expression Regulation
  • Genes, myc / genetics
  • Genes, ras / genetics
  • Humans
  • Hypoxanthine Phosphoribosyltransferase / genetics
  • Ki-67 Antigen / genetics
  • Mammary Neoplasms, Experimental / genetics*
  • Mammary Neoplasms, Experimental / pathology
  • Mice
  • Mice, Transgenic
  • Ornithine Decarboxylase / genetics
  • Protein Precursors / genetics*
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Receptor, ErbB-2 / genetics
  • Thymosin / analogs & derivatives*
  • Thymosin / genetics
  • Transgenes
  • Tumor Cells, Cultured

Substances

  • Cyclin B
  • Cyclin E
  • Ki-67 Antigen
  • Protein Precursors
  • RNA, Messenger
  • prothymosin alpha
  • Cyclin D1
  • Thymosin
  • Hypoxanthine Phosphoribosyltransferase
  • Receptor, ErbB-2
  • Ornithine Decarboxylase