Abstract
Background
Multiple factors have been shown to delay dermal wound healing. These resultant wounds
pose a significant problem in terms of morbidity and healthcare spend. Recently, an
increasing volume of research has focused on the molecular perturbations underlying
non-healing wounds.
Objectives
This study investigates the effect of a novel cancer promoter, Ehm2, in wound healing.
Ehm2 belongs to the FERM family of proteins, known to be involved in membrane–cytoskeletal
interactions, and has been shown to promote cancer metastasis in melanoma, prostate
cancer and breast cancer.
Methods
Ehm2 mRNA levels were analysed using qRT-PCR, standardised to GAPDH, from either acute
or chronic wounds, and normal skin. IHC analysis was also undertaken from wound edge
biopsies. An anti-Ehm2 transgene was created and transfected into the HaCaT cell line.
The effect of Ehm2 knockdown on migration, adhesion, growth, cell cycle progression
and apoptosis was analysed using standard laboratory methods. Western Blot analysis
was used to investigate potential downstream protein interactions.
Results
Ehm2 is expressed nearly three times higher in acute wound tissues, compared to chronic
wound tissues. Increased Ehm2 expression is found in wounds undergoing healing, especially
at the leading wound edge. In vitro, Ehm2 knockdown reduces cellular adhesion, migration
and motility, without affecting growth, cell cycle and apoptosis. Finally, Ehm2 knockdown
results in reduced NWasp protein expression.
Conclusion
These results suggest Ehm2 may be an important player in the wound healing process,
and show that Ehm2 knockdown downregulates the expression of NWasp, through which
it may have its effect on cellular migration.
Keywords
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Article info
Publication history
Published online: May 13, 2013
Accepted:
April 4,
2013
Received in revised form:
March 17,
2013
Received:
December 15,
2012
Identification
Copyright
© 2013 Japanese Society for Investigative Dermatology. Published by Elsevier Inc. All rights reserved.
