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Title: PRG4 expression in myxoid liposarcoma maintains tumor cell growth through suppression of an antitumor cytokine IL-24

Journal Article · · Biochemical and Biophysical Research Communications
 [1];  [1];  [2];  [1];  [1];  [2];  [1]
  1. Department of Pathology, Wakayama Medical University, 811-1 Kimiidera, Wakayama-shi, Wakayama 641-8509 (Japan)
  2. Department of Molecular Pathology, Tokyo Medical University, 6-1-1 Shinjuku, Shinjuku-ku, Tokyo 160-8402 (Japan)

PRG4 is one of the downstream molecules of the myxoid liposarcoma (MLS)-specific fusion oncoproteins TLS-CHOP and EWS-CHOP. Exogenous PRG4 expression increases the tumorigenicity of cells injected in nude mice. The molecular functions of PRG4 in tumorigenesis and/or tumor progression of MLS cells, however, still remain unclear. In this report, we demonstrated that siRNA-mediated knockdown of PRG4 suppressed the growth of the MLS-derived cell lines 1955/91 and 2645/94. In addition, PRG4 knockdown promoted adipocytic differentiation in 1955/91 cells. Thus, PRG4 may play essential roles in MLS cell growth and have potential as a therapeutic target. On the other hand, our previous study has revealed that TLS-CHOP suppresses expression of an anti-tumor cytokine IL-24, contributing to tumor cell survival. In this study, we found that double knockdown of PRG4 and IL-24 did not inhibit MLS cell growth, and single knockdown of PRG4 remarkably increased IL-24 expression. These results suggest that the growth inhibitory effect of PRG4 knockdown is caused by induction of IL-24 expression, and PRG4 may contribute to maintain MLS cell growth through repression of IL-24 expression. - Highlights: • PRG4 knockdown suppresses growth of myxoid liposarcoma cells. • Unscheduled expression of PRG4 may inhibit adipogenesis in myxoid liposarcoma cells. • PRG4 may has potential as a therapeutic target for myxoid liposarcoma. • PRG4 represses an anti-tumor cytokine IL-24, maintaining myxoid liposarcoma cells.

OSTI ID:
22696931
Journal Information:
Biochemical and Biophysical Research Communications, Vol. 485, Issue 1; Other Information: Copyright (c) 2017 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
Country of Publication:
United States
Language:
English

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