Fig. 7: BITC inactivates the PI3K/AKT signaling pathway through inhibition of MTA2 in PDAC cells.

a MIA PaCa-2 or PANC-1 cells were treated with varying concentrations of benzyl isothiocyanate (BITC) or dimethyl sulfoxide (as a vehicle control) for 0, 8, 16, and 24 h. Cell proliferation was evaluated by CCK-8 assays. Data are expressed as mean ± S.D. n = 3. *P < 0.05, **P < 0.01. b MIA Paca-2 or PANC-1 cells were treated with different concentrations of BITC for 24 h, and the whole-cell lysates were subjected to western blot analysis. The protein levels of MTA2, PTEN, phosphorylated PI3K (p-PI3K), PI3K, p-AKT, and AKT were measured. c MIA Paca-2 or PANC-1 cells were treated with 10 μmol/L BITC for the specified durations. The protein levels of MTA2, PTEN, p-PI3K, PI3K, p-AKT, and AKT were measured using western blot. d Proposed model for the role of MTA2 in PDAC cells. PTEN is identified as one of the genomic targets of MTA2/NuRD, and PTEN suppression by MTA2 is recruited by Snail. The mechanism of MTA2-mediated PDAC cell proliferation, migration, and invasion is due to the noted repression of PTEN and activation of the PI3K/AKT signaling pathway. In addition, MTA2 works as the molecular target of BITC in the human pancreatic cancer cells