Leucine aminopeptidase may contribute to the intrinsic resistance of cancer cells toward cisplatin as revealed by an ultrasensitive fluorescent probe

) and combining it with confocal fluorescence imaging, we analyze the concentration change of LAP in cancer cells such as HepG2 and A549 cells under cisplatin treatment. We find that a large increase in the LAP concentration occurs in HepG2 rather than in A549 cells. These different changes are further confirmed by an ELISA kit. A cell viability assay reveals that HepG2 cells with a higher level of LAP have much stronger resistance toward cisplatin than A549 cells, suggesting that LAP may serve as a simple indicator to reflect the relative resistance of different cancer cells. Importantly, inhibiting the expression of LAP with siRNA further decreases cell viability. These findings support that LAP may contribute to the intrinsic resistance of cancer cells toward cisplatin. In addition, the proposed probe may find more uses in studying the cellular LAP function, and improving chemotherapeutic cancer treatment.