In vitro study reveals the loss of complex glycolipids in transformed hamster cells, suggesting that normal contact inhibition is required for complex glycolipid synthesis.
The synthesis of glycolipids by the NIL2 hamster line and transformed NIL2 lines has been studied by measuring the incorporation of palmitate-I-14C into cellular lipids. Although ceramide monohexoside (CMH) ceramide dihexoside (CDH) and haematoside are present at comparable levels in NIL2 cells and transformed NIL cells it has been found that three larger glycolipids are absent from transformed lines. These same three lipids and only these three are present at a lower level in actively growing NIL2 cells than in contact inhibited NIL2 cells. It is concluded that the lack of some or all of the manifestations of contact inhibition may be important in the depression of complex glycolipid synthesis in either normal or transformed cells. Put in another way, it may be that some phase of normal contact inhibition serves as a positive control that increases the accumulation of one or more of the complex glycolipids of the cell. Lack of normal contact inhibition for any reason (e. g. transformation or lack of contact) results in lower levels of complex glycolipids. The specific lipids involved may vary from one cell line to another. No mechanism for the effect is proposed.
No takes yet. Share an insight, caveat, or question.
Robbins et al. (1971) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: