Supplementary Materials for:
Chronic Activation of mTOR Complex 1 Is Sufficient to Cause
Hepatocellular Carcinoma in Mice
Suchithra Menon, Jessica L. Yecies, Hui H. Zhang, Jessica J. Howell, Justin Nicholatos,
Eylul Harputlugil, Roderick T. Bronson, David J. Kwiatkowski, Brendan D. Manning*
*To whom correspondence should be addressed. E-mail: bmanning{at}hsph.harvard.edu
This PDF file includes:
- Fig. S1. mTORC1 signaling is increased in the livers of obese mice, and LTsc1KO mice exhibit sustained mTORC1 signaling under fasting conditions.
- Fig. S2. LTsc1KO female mice also develop HCC.
- Fig. S3. LTsc1KO mice are protected from age-related hepatic steatosis.
- Fig. S4. Status of pathways that contribute to HCC and metabolic proteins in normal
and tumor tissue of LTsc1KO livers.
- Fig. S5. Changes in LTsc1KO livers at 6 months of age before the appearance of
tumors.
- Fig. S6. Long-term rapamycin treatment of LTsc1KO mice decreases mTORC1
signaling, proliferation, apoptosis, inflammation, progenitor cell expansion, and
DNA damage in the liver.
- Fig. S7. Cytostatic, but not cytotoxic, response of LTsc1KO liver tumors to
rapamycin and inhibition of mTORC1 signaling by rapamycin in tumor regions
resistant to rapamycin.
- Fig. S8. ER stress and defective mitochondria in LTsc1KO livers before the
appearance of tumors.
- Table S1. RT-PCR primers used in this study.
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Citation: S. Menon, J. L. Yecies, H. H. Zhang, J. J. Howell, J. Nicholatos, E. Harputlugil,
R. T. Bronson, D. J. Kwiatkowski, B. D. Manning, Chronic Activation of mTOR Complex 1 Is Sufficient to Cause
Hepatocellular Carcinoma in Mice.
Sci. Signal. 5, ra24 (2012).
© 2012 American Association for the Advancement of Science
