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L A Smets

Publications and source records attributed to L A Smets.

95 records · Page 6Linked to original sources
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Effect of temperature on invasion of MO4 mouse fibrosarcoma cells in organ culture.

Invasion by MO4 mouse fibrosarcoma cells into fragments of embryonic chick heart or lung in organ culture was studied histologically and ultrastructurally at various temperatures between 12 and 40 degrees C. Invasion was absent for at least 7 days at or below temperatures of 29 degrees C. Invasion was invariably observed at or above 30.5 degrees C. Differences in invasion between 29 and 30.5 degrees C could not be ascribed to differences in growth, migration, or microtubule assembly/disassembly of MO4 cells. Neither could they be explained through differences in the attachment of MO4 cells to the heart fragments. Possible explanations for the absence of invasion at lower temperature are: altered resistance of the extracellular matrix in heart or lung fragments, and deficient expression of fucosylated glycoproteins at the surface of MO4 cells. A population of MO4 cells plated from the parent line and adapted to grow at 28 degrees C (MO(4)28 cell line) did not differ in invasiveness from the parent MO4 cells. We conclude that the temperature dependence of invasion in organ culture might indicate as yet unexplored aspects of the mechanisms of tumour invasion.

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Restored invasion of mouse MO4 cells into chick heart in vitro through mutual conditioning at reduced temperature.

Invasion of malignant mouse MO4 cells into embryonic chick heart fragments in confronting organ cultures was arrested for 7 days when the temperature of incubation was lowered to 28 degrees C. Afterwards invasion resumed and progression between days 10 and 17 at 28 degrees C was comparable to that between days 0 and 7 at 37 degrees C. This pattern of progression of MO4 cell invasion at 28 degrees C was unaltered when either MO4 cells or heart fragments or both were preincubated separately at 28 degrees C for 14 days before confrontation with each other. Invasion at 28 degrees C resumed only when MO4 cells and heart tissue had been in immediate contact for at least 7 days. Metabolic labelling with [3H]fucose showed a correlation in time between transient suppression of invasion and transient inhibition of incorporation of fucosylation-precursor molecules into glycoproteins by MO4 cells. The latter activity was far less temperature-sensitive in heart cells. Our observations suggest that metabolic cooperation between invading MO4 cells and heart tissue is essential for progression of invasion in vitro.

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Decreased fucose incorporation in cell surface carbohydrates is associated with inhibition of invasion.

Invasion of malignant MO4 cells into embryonic chick heart fragments in an organ culture assay was arrested for at least 7 days when the temperature was lowered to 28 degrees C. Prolonged culturing of MO4 cells at 28 degrees C on tissue culture substrates showed no recuperation of fucose incorporation into cell surface glycopeptides. However, invasion was restored after 10 days of organ culture in confrontation with chick heart tissue at 28 degrees C. A histoautoradiographic study showed that the regained capability to invade was accompanied by an increase in fucose labeling of the MO4 cells in the invading areas. At 28 degrees C the incorporation of [3H]fucose into total cell protein was drastically reduced, whereas [3H]leucine incorporation as a measure for protein synthesis was less affected. Cell surface glycopeptides, metabolically labeled with either fucose or glucosamine at 28 degrees C, showed a time-dependent decrease in the incorporation of fucose but not of glucosamine and no changes in overall size distribution. Low temperature did not reduce fucosyltransferase activity but the relative accumulation of fucose-1-P suggested inhibited conversion towards GDP-fucose. Moreover, mouse L cells which were incapable of invading chick heart tissue appeared also deficient in fucose incorporation, owing to low levels of fucosyltransferase activity. According to the results, fucosylation of surface carbohydrates may be required for invasive capacity and restored in MO4 cells invading at 28 degrees C by metabolic cooperation with the host tissue.

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