Table 1 NDPKs may affect cell migration in a dosage-dependent manner

	Loss of NDPK	Heterozygote	Overexpression
D. melanogaster (border cell migration)	No migration	Low level of AWD: migration	No migration
D. melanogaster (tracheal cell migration)	Disrupted structures	Ectopic migration	?
*C. elegans* (DTC migration)	Incomplete migration	Ectopic migration	Incomplete migration
MDA-MB231T—human invasive breast carcinoma cell line (migratory potential)	?	High migratory potential—endogenous level of NM23-H1 is low	Low migratory potential when NM23-H1, NM23-H2 or NDK-1 overexpressed

Most data were described in the fruit fly and in human cell lines. In C. elegans our group examined the effect of different NDPK levels (eg, absence of NDK-1, half dosage and excess NDK-1) exerted on the migration of distal tip cells. We propose that different dosage of NDPKs alters cell migration phenotypes in different models and cell types in a similar way: (1) The absence of NDPKs causes the most severe morphological defects in the two model organisms such as disrupted tracheal structures, stalled border cell migration in the fly and underdeveloped gonad arms in the worm due to insufficient migration. (2) Half dosage of NDPKs leads to ectopic migratory phenotypes, such as ectopic tracheal branches and gonadal extra turns or overshoots. In MDA-MB231T highly invasive breast carcinoma cells endogenous NM23 level is low. (3) An elevated NDPK level also leads to incomplete gonadal migration in the worm due to a premature stop of DTCs in the third phase of migration, where NDK-1 acts. Excess AWD causes stalled migration of border cells. In MDA-MB231T cells excess of NM23-H1/2 or NDK-1 results in inhibition of migratory potential. Expressions labelled by bold are C. elegans specific terms.

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