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. 2019 Feb 27;54(5):1591–1600. doi: 10.3892/ijo.2019.4728

Figure 5.

Figure 5

Chemoresponse to epirubicin is dependent on the PI3K/AKT/CREB/apoptosis axis, which is regulated by MRPL33-L and MRPL33-S in gastric cancer cells. (A) Western blot analysis and (B) corresponding histogram of ratio of p-AKT/AKT, ratio of p-CREB/CREB, Mcl-1 and Bcl-2 expression levels in the AGS cell groups (control, plenti-vector-plentil-MRPL33-S and plenti-MRPL33-L-transfected), with or without 0.3 µM epirubicin. (C) Western blot analysis and (D) corresponding histogram of ratio of p-AKT/AKT, ratio of p-CREB/CREB, Mcl-1 and Bcl-2 expression levels in the MGC-803 cell groups (control, plenti-vector, plentil-MRPL33-S and plenti-MRPL33-L), with or without 0.3 µM epirubicin. (E) Histograms of chemoresponse in AGS cell groups and (F) MGC-803 cell groups treated with 0.3 µM epirubicin for 72 h. Three independent biological replicates were performed and data were presented as the mean ± standard deviation. *P<0.05, **P<0.01 and ***P<0.001 with comparisons shown by brackets. PI3K, phosphoinositide 3-kinase; AKT, AKT serine/threonine kinase; CREB, cAMP response element-binding protein; MRPL33, mitochondrial ribosomal protein L33; L, long variant; S, short variant; p-, phosphorylated; Mcl-1, myeloid cell leukemia 1; Bcl-2, B-cell lymphoma 2.