Assimilation of LDL by experimental tumours in mice

Biochim Biophys Acta. 1989 Jun 28;1003(3):301-6. doi: 10.1016/0005-2760(89)90236-1.

Abstract

We have studied the uptake of 125I-labelled low-density lipoprotein (LDL) by seven experimental murine tumours in vivo. Four tumours (Lewis Lung carcinoma, B-16, MS-2 and Colon 26) showed a higher relative uptake of lipoprotein as compared to the liver, two (L-1210 and P-388) had a very low lipoprotein uptake, while lipoprotein uptake by tumour M5 was similar to that of the liver. The data was confirmed by tracing tissue uptake of lipoproteins using [14C]sucrose-labeled LDL. These in vivo findings correlated well with the in vitro specific binding of 125I-beta-VLDL to membranes prepared from tumours, thus suggesting that the expression of the LDL receptor in the tumours is related to the in vivo uptake of lipoprotein. Further analysis of the LDL receptor by ligand blotting showed that the tumor receptor has several of the liver LDL receptor characteristics (including apparent Mr, sensitivity to proteinases, and Ca2+ requirement of lipoprotein binding). In summary, our data show that experimental murine tumours express the LDL receptor and suggest that the high relative in vivo uptake of LDL is determined by the elevated LDL-receptor expression in the tumours.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Biological Transport
  • Cell Membrane / metabolism
  • Edetic Acid / pharmacology
  • Kinetics
  • Lipoproteins, LDL / metabolism*
  • Lipoproteins, VLDL / metabolism
  • Liver / metabolism
  • Mercaptoethanol / pharmacology
  • Mice
  • Neoplasms, Experimental / metabolism*
  • Pronase / pharmacology
  • Receptors, LDL / metabolism*

Substances

  • Lipoproteins, LDL
  • Lipoproteins, VLDL
  • Receptors, LDL
  • Mercaptoethanol
  • Edetic Acid
  • Pronase