We have shown previously that cytosolic tyrosine kinase Src is involved in EGFR transactivation in HBEC exposed to another oxidant stressor (Wu et al.
3]-induced EGFR transactivation at both transphosphorylation and autophosphorylation sites in HBEC.
To determine whether Src-mediated EGFR (Y1068) phosphorylation is EGFR kinase-dependent, we pretreated BEAS-2B cells (Figure 5A) or ALI-cultured primary HBEC (Figure 5B) with vehicle (0.
3] results in increased expression of proinflammatory mediators, including IL-8 in HBEC (Bayram et al.
Akt but not Erkl/2 activation enables As-transformed HBEC migration and invasion.
Together, these results indicate that Akt activation drives As-transfonned HBEC migration and invasion mainly through promoting ZEBl and ZEB2 expression.
In the present study, we provided additional novel evidence suggesting that abnormal cell signaling and gene expression may play a crucial role in arsenic lung carcinogenesis by promoting As-transformed HBEC migration and invasion.
While EMT is generally considered a late event in cancer progression, our and other recent findings provide evidence that EMT may also play a role in arsenic-caused or tobacco-carcinogen--caused HBEC transformation, the initial step of carcinogenesis (Tellez et al.
4] were performed using HBECs from six different individuals.
In the present study we first determined the differential gene expression patterns in HBECs exposed to 50 [micro]M of V and Zn and found 140 and 76 genes altered by V and Zn, respectively, compared with control.
Vanadium also increased the expression of DTR [heparin-binding epidermal growth factor-like growth factor (HB-EGF)] in HBECs and fibroblasts (Ingrain et al.
Our study compared gene expression profiles induced by V and Zn in HBECs and identified a group of 12 genes and several metallothionein 1 genes that may be used as a biomarker for V and Zn exposure, respectively.