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. 2016 Feb 16;7(12):14300–14309. doi: 10.18632/oncotarget.7426

Figure 4. RACK1 reactivates the ERK and Akt pathways during induction of imatinib resistance in GIST cells.

Figure 4

A. GIST-882 and GIST-T1 cells were harvested after imatinib treatment for the indicated times, and whole cell lysates were analyzed by Western blotting for RACK1, p-c-KIT, total c-KIT, p-ERK, total ERK, p-AKT, and total AKT. B. GIST-T1 and GIST-882 cells were transfected with control or RACK1 siRNAs. Transfected cells were cultured for 72 hours and harvested after imatinib treatment for 2 or 4 days. Whole cell lysates were subjected to Western blot to determine the protein levels of RACK1, p-c-KIT, total c-KIT, p-ERK, total ERK, p-AKT, and total AKT. C. GIST-T1 and GIST-882 cells were transfected with pcDNA3.0/RACK1 or control vector, after which whole cell lysates were analyzed by Western blotting for p-c-KIT, total c-KIT, p-ERK, total ERK, p-AKT, and total AKT. D. Cell lysates from imatinib-resistant sublines of GIST-882 cells were subjected to immunoprecipitation with anti-RACK1 antibody, followed by Western blot with related antibodies as indicated.