ZFIN Image: Nguyen et al., 2012, Fig. 4

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Fig. 4

Suppression of liver tumorigenesis by inhibition of the Raf-MEK-ERK and PI3K-AKT-mTOR pathways. (A) Fluorescent images showing representative mifepristone-induced EGFP-kras^V12 driver-effector larvae at 7 dpf treated with different inhibitors, as compared with the DMSO-treated driver and driver-effector transgenics as controls. Scale bar: 200 μm. (B) Comparison of the anti-HL effect of inhibitors in transgenic larvae at 7 dpf. The liver size of treated larvae was classified as ‘normal’ if it was the same as the liver in driver transgenics, ‘huge’ if it remained enlarged/hyperplasia, or ‘large’ if it was larger than normal liver, but smaller than hyperplasia after 4 days of inhibitor treatment. (C) Lysates extracted from whole transgenic larvae treated with the indicated inhibitors were immunoblotted for phospho-ERK (P-ERK), P-AKT and P-S6. β-actin, internal control for equal loading. (D) Proposed inhibitor treatments to suppress Kras^V12-induced liver tumorigenesis via targeting both the Raf-MEK-ERK and PI3K-AKT-mTOR pathways.

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Acknowledgments

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