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Cell migration and MMP‐9 secretion are increased by epidermal growth factor in HaCa T‐ ras transfected cells
Author(s) -
Charvat Sandrine,
Chignol MarieChristine,
Souchier Catherine,
Griel Caroline Le,
Schmitt Daniel,
Serres Mireille
Publication year - 1998
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/j.1600-0625.1998.tb00322.x
Subject(s) - hacat , epidermal growth factor , transfection , cell culture , cell growth , keratinocyte , motility , cell migration , microbiology and biotechnology , biology , cell , cancer research , chemistry , biochemistry , genetics
Mutated RAS oncoproteins and epidermal growth factor (EGF) are thought to contribute to the proliferative, invasive and metastatic properties of transformed cells. In the present study, we investigated the role of EGF in two H‐ ras transfected clones and compared it to that in the parental cell line, HaCaT and primary cultured keratinocytes. Our findings show that the motility on type I collagen, measured by the migration index, was similar for both the HaCaT cell line and normal human keratinocytes, whereas it was higher for the HaCaT‐ ras clones. These results suggest an involvement of the ras oncogene in the stimulation of cell migration. EGF, in cell pretreatment or during the migration assay also caused an increase in migration of all the cells, but preserved the difference between HaCaT and HaCaT‐ ras . However, no significant difference in EGF‐R expression was detected between normal cultured keratinocytes, HaCaT and HaCaT‐ ras cell lines with or without EGF pretreatment. Moreover, when the cells were stimulated with EGF, the MMP‐9 activity was greatly increased in a dose‐dependent manner in all the cells, and EGF stimulation particularly highlights the increased amount of MMP‐9 in HaCaT‐ ras cells compared to HaCaT cells. In conclusion, EGF is able to enhance motility and to up‐regulate MMP‐9 activity in all cells, but with a higher impact in HaCaT‐ ras cells without an overexpression of EGF‐R. As EGF acts in synergy with the H‐ ras mutation, they could be implicated in the local invasion by the HaCaT‐ ras clones.