Skip to main content
. 2018 Jan 16;15(3):3883–3889. doi: 10.3892/ol.2018.7800

Figure 3.

Figure 3.

Increased HSPA12B induces chemoresistance in NSCLC cells by modulating PI3K/Akt/NF-κB signaling pathway and apoptosis-associated proteins. (A) In the CDDP-treated A549/HSPA12B+/+ solid tumors, the expression of p-IκBα, p-Akt and Bcl-2 were significantly increased while cleaved caspase-3 expression was significantly decreased compared with CDDP-treated A549 tumors. (B) The PI3K inhibitor LY294002, Akt inhibitor triciribine and NF-κB inhibitor CAPE significantly increased cleaved caspase-3 expression and inhibited the Bcl-2 level in HSPA12B+/+ cells compared with the control groups. Data are presented as the mean ± standard deviation. *P<0.05 vs. HSPA12B+/+. CDDP, cisplatin; HSPA12B, heat shock protein family A member 12B; PI3K, phosphoinositide 3-kinase; Akt, protein kinase B; NF-κB nuclear factor-κB; p-, phosphorylated; IκBz, nuclear factor of κ light polypeptide gene enhancer in B-cells inhibitor, α; CAPE, caffeic acid phenethyl ester; Bcl-2, B-cell lymphoma 2.