The BEAS-2B cell line was derived by transforming HBEC with an adenovirus 12-simian virus 40 construct (Reddel et al.
3] exposure and induction of phosphorylation of EGFR (Y1068) in HBEC.
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.
Stable reexpresson of miR-200b completely inhibits As-transformed HBEC migration and invasion.
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.
HBECs were lysed in guanidine isothiocyanate (GITC) buffer [4 M GITC (Boehringer Mannheim, Indianapolis, IN), 25 mM sodium citrate (pH 7.
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.