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. Author manuscript; available in PMC: 2010 Dec 21.
Published in final edited form as: Oncogene. 2010 Aug 9;29(42):5741–5754. doi: 10.1038/onc.2010.309

Figure 2.

Figure 2

MUC4 expression induces upregulation of N-cadherin via FAK signaling. (a) Immunoblot analysis showed an increase in the activation of FAK, MKK7, JNK1/2, c-Jun and upregulate N-cadherin in SKOV3-MUC4 cells as compared with vector control cells. The total form of FAK, MKK7, JNK1/2, c-Jun molecules remains unchanged in both cell lines. β-actin was used as a loading control. (b) Treatment with pFAK inhibitor: Immunobloting analysis of pFAK and FAK in cells treated with 10 and 50 μm FAK inhibitor (FAK inhibitor-14 (1,2,4,5-benzenetetraamine tetrahydrochloride)-treated SKOV3-MUC4 cells. (c) Western blot analysis showed that the inhibition of pFAK reduces the activation of FAK, MKK7, JNK1/2, c-Jun and decreases the expression of N-cadherin. The total form of FAK, MKK7, JNK1/2, c-Jun molecules remains the same. β-actin was used as a loading control. (d) Inhibition of pJNK1/2: immunoblotting analysis showing the expression of pJNK, JNK and N-cadherin in JNK1/2 inhibitor (SP600125; 20, 40 and 80 nm)-treated SKOV3-MUC4 cells. β-actin was used as a loading control.