Abstract
BackgroundIntegrin-linked kinase (ILK) is a ubiquitously expressed protein kinase that has emerged as one of the points of convergence between integrin- and growth factor-signalling pathways.ResultsIn this study we identify the ILK isoform expressed in five human oesophageal squamous cell carcinoma cell lines of South African origin as ILK1, and demonstrate its cellular distribution. ILK expression, although similar in the majority of the cell lines, did show variation. Furthermore, the ILK expressed was shown to be catalytically functional. The effect of growth factors on ILK expression was examined. An increase in ILK expression, following EGF and TGFβ1 exposure, was a trend across all the five oesophageal carcinoma cell lines tested.ConclusionThese results suggest that growth factor modulation of ILK expression relies on the internalisation/recycling of growth factor receptors and stimulation of the PI3K pathway, which may have implications with regards to cell adhesion and tumourigenesis.
Highlights
Integrin-linked kinase (ILK) is a ubiquitously expressed protein kinase that has emerged as one of the points of convergence between integrin- and growth factor-signalling pathways
Digestion of the ILK fragment did not occur with the HincII restriction enzyme (Figure 2B) confirming that these oesophageal SCC cell lines only express the ILK1 isoform
Densitometric analysis revealed that ILK expression levels were comparatively similar across the WHCO3, WHCO5 and SNO cell lines
Summary
Integrin-linked kinase (ILK) is a ubiquitously expressed protein kinase that has emerged as one of the points of convergence between integrin- and growth factor-signalling pathways. While responsiveness to growth factors is central to a host of normal cellular events, aberrant activity plays a key role in tumour development [1,2,3]. The action of EGF has been implicated in malignant transformation in squamous cancers of the bladder, breast and lung [5], whereas colon, gastric, endometrial, ovarian and cervical malignancies exhibit loss of response to TGFβ1 as a growth inhibitor [6,7]. The response to growth factors can be potentiated by the integrin class of adhesion receptors through the integrin-associated protein, integrin-linked kinase (ILK) [1,7,11]
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