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. Author manuscript; available in PMC: 2013 May 6.
Published in final edited form as: Int J Cancer. 2009 Aug 15;125(4):942–951. doi: 10.1002/ijc.24424

Figure 2. The induction of apoptosis by TAT-CTMP4 occurs via inhibition of the AKT pathway.

Figure 2

(A) Model human pancreatic adenocarcinoma (CFPAC-1) were treated with escalating doses of TAT-CTMP4. Samples were treated for 1 hour prior to preparation of cell lysates. Western blots were subsequently prepared and stained with anti-total AKT and anti-phospho-AKT (Ser473). (B) Panc-1 lysates were generated after exposure to PBS (no treatment control), DMSO (vehicle control for wortmannin), wortmannin (1 µM), TAT-CTMP4-Inactive (10 µM), and TAT-CTMP4 (10 µM) for 18 hours. Western blots were probed with anti-total GSK-3β and phospho-GSK-3α/β (Ser21/9). (C) Human model pancreatic adenocarcinoma (CFPAC-1) were treated with PBS (no treatment), gemcitabine (30 nM), recombinant human TNF-α (10 ng/ml), wortmannin (1 µM), TAT-CTMP4-Inactive (10 µM), and TAT-CTMP4 (10 µM). One hour later, cell lysates were generated and phospho-proteins were quantitated by bioplex analysis. Each experimental group represents an n=4. Results are expressed as the mean, with bars representing standard error of the mean.