LiSa-2, a novel human liposarcoma cell line with a high capacity for terminal adipose differentiation

Int J Cancer. 2000 Dec 15;88(6):889-94. doi: 10.1002/1097-0215(20001215)88:6<889::aid-ijc8>3.0.co;2-n.

Abstract

LiSa-2 is a stable cell line derived from a poorly differentiated, pleomorphic liposarcoma. In serum-containing medium, LiSa-2 cells are fibroblastoid and rapidly dividing. In a serum-free, chemically defined culture medium containing physiological concentrations of insulin, triiodothyronine and cortisol, LiSa-2 cells divide slower and, extensively storing fat, acquire adipocyte morphology. In contrast to fibroblastoid LiSa-2 cells, these adipocyte-like LiSa-2 cells highly express transcripts for peroxisome proliferator-activated receptor-gamma, lipoprotein lipase, fatty acid synthetase, hormone-sensitive lipase, adipocyte most abundant gene transcript-1, glycerol-3-phosphate-dehydrogenase and the insulin-sensitive glucose transporter-4, all of which are specific for differentiated adipocytes. However, leptin mRNA expression was demonstrated only after preventing DNA methylation by incorporation of 5-aza-deoxycytidine into cellular DNA. Functionally, adipocyte-like LiSa-2 cells show increased insulin-dependent glucose uptake and lipid synthesis and are sensitive to lipolytic agents. This cell line may serve as an in vitro model for studying the regulation of human liposarcoma differentiation and for screening drugs for induction of differentiation-associated growth arrest in liposarcomas.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipocytes / cytology*
  • Cell Differentiation / physiology
  • Cell Division / physiology
  • Culture Media
  • Humans
  • Karyotyping
  • Liposarcoma / genetics
  • Liposarcoma / metabolism*
  • Liposarcoma / pathology
  • Male
  • Middle Aged
  • Receptors, Cytoplasmic and Nuclear / metabolism*
  • Transcription Factors / metabolism*
  • Tumor Cells, Cultured / cytology
  • Tumor Cells, Cultured / metabolism*

Substances

  • Culture Media
  • Receptors, Cytoplasmic and Nuclear
  • Transcription Factors