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. Author manuscript; available in PMC: 2012 Feb 1.
Published in final edited form as: Cancer Res. 2010 Dec 8;71(3):1019–1028. doi: 10.1158/0008-5472.CAN-10-1855

Figure 5. MT1-MMP expression attenuates gemcitabine-induced checkpoint arrest by inducing ERK1/2 phosphorylation and HMGA2 expression.

Figure 5

A. Panc1 and CD18 cells inducibly expressing vector (V) or full-length MT1-MMP were grown in collagen, treated with gemcitabine for 24 hours and immunoblotted for pS345Chk1. B. Panc1 cells expressing V, full-length MT1-MMP or tail-less mutant of MT1-MMP (ΔC) were grown in collagen and immunoblotted for ppERK1/2 and HMGA2. C. Panc1-MT cells grown in collagen were treated with gemcitabine and co-treated with DMSO or U0126 and analyzed for pS345Chk1 and ppERK1/2 expression. D. Panc1-MT cells transfected with control or HMGA2 siRNA (50 nM) were plated in collagen before treating with gemcitabine for 24 hours and immunoblotted for pS345Chk1. E. De-identified PDAC samples (n=21) were procured on an IRB-approved protocol. The cancerous and adjacent normal tissue samples were processed for MT1-MMP and HMGA2 mRNA by qRT-PCR and the relationship between MT1-MMP and HMGA2 was analyzed using Spearman’s rank correlation coefficient.