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. 2012 Jun 5;303(3):E410–E421. doi: 10.1152/ajpendo.00039.2012

Fig. 7.

Fig. 7.

STAT3 inhibition using dnSTAT3 or short hairpin (sh)STAT3 prevented C26 tumor-induced muscle atrophy in mice. Mice were transfected on the day of tumor inoculation and euthanized 12 days later. A: CMV-dnSTAT3 transfection of tibialis anterior muscle resulted in basal hypertrophy in non-tumor-bearing mice and reduced muscle wasting in C26 tumor-bearing mice vs. CMV-empty vector transfected controls (n = 250–500 fibers from n = 8 mice/condition, repeated twice). B: immunohistochemistry (brown staining; top) and immunofluorescence (bottom) for pY705-STAT3 in tibialis anterior muscles electroporated with CMV-dnSTAT3. Note pSTAT3 nuclear localization is reduced in the presence of dnSTAT3 (brown staining in immunohistochemistry, red staining in immunofluorescence analyses). C: CMV-dnSTAT3 transfection decreased STAT3 DNA-binding activity in nuclear extracts derived from transfected tibialis muscle in mice with C26 cachexia, as shown by the electrophoretic mobility shift assay (EMSA; n = 6/condition). §Unlabeled probe control. D: Western blotting analysis of total lysate from tibialis of control (non-tumor-bearing) and C26 tumor-bearing mice transfected with CMV-dnSTAT3 or empty vector shows expression of the Flag-taged-dnSTAT3 and GFP, with GAPDH as loading control (n = 4). E: CMV-shSTAT3 increased muscle CSA and prevented C26-induced fiber wasting in the tibialis muscle vs. CMV-shScramble (n = 1,650–2,750 fibers from n = 8 mice/condition, repeated twice). ***P < 0.001.