p53 overexpression and downregulation of inter-α-inhibitor are associated with hyaluronidase enhancement of TNF cytotoxicity in L929 fibroblasts

Nan Shan Chang, Gregory Carey, Nicole Pratt, Elaina Chu, Melody Ou

Research output: Contribution to journalArticlepeer-review

11 Citations (Scopus)

Abstract

Degradation of extracellular matrix by hyaluronidase increases murine L929 cell sensitivity to tumor necrosis factor (TNF) cytotoxicity. Seeding and culturing L929 cells onto the matrix of serum fetuin and the hyaluronate-binding inter-α-inhibitor resulted in inhibition of hyaluronidase-enhanced TNF killing, suggesting that the release of these proteins from hyaluronidase-degraded matrix confers cellular TNF susceptibility. Metabolic labeling studies showed that hyaluronidase mediated de novo protein synthesis and downregulated several proteins in L929 cells. Specifically, hyaluronidase upregulated p53 protein expression (>200%) but downregulated a p85 inter-α-inhibitor-like protein (>90%) in L929 cells, whereas it had no effect on the protein levels of ICH-1, Bcl-xL, Bcl-2, Fas ligand, CAS (cellular apoptosis susceptible protein), TIAR (an RNA-binding protein) and α-tubulin. Conceivably, hyaluronidase enhancement of TNF sensitivity in L929 cells is p53-dependent and the matrix inter-α-inhibitor contributes a protective role against TNF cytotoxicity. Copyright (C) 1998 Elsevier Science Ireland Ltd.

Original languageEnglish
Pages (from-to)45-54
Number of pages10
JournalCancer Letters
Volume131
Issue number1
DOIs
Publication statusPublished - 1998 Sep 11

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research

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