The present study aimed to reveal the association between
insulin-like growth factor binding protein-2 (IGFBP-2) and the sensitivity of
bladder cancer cells to
cisplatin, and determine the underlying mechanism involving
maspin. A total of 32
bladder cancer tissue samples were collected for analysis. Cells of the BIU87 human
bladder cancer cell line were cultured and a
cisplatin-resistant subline (BIU87-CisR) was established by continuous exposure of the cells to
cisplatin. Targeted inhibition of
IGFBP-2 in the BIU87-CisR cells was performed using
small interfering RNA technology. The expression levels of
IGFBP-2 and
maspin in the tissue samples and cells were analyzed using reverse transcription-quantitative polymerase chain reaction and western blot analyses. Cell viability following treatment in each group was evaluated using a Cell Counting Kit-8 assay subsequent to treatment with 3 μM
cisplatin. The cell cycle and apoptotic rate of the BIU87-CisR cells were analyzed using flow cytometry. Finally,
maspin-overexpressing BIU87-CisR cells were used to confirm the effect of
maspin on the sensitivity of the cells to
cisplatin. The expression levels of
IGFBP-2 in chemoresistant patients and BIU87-CisR cells were significantly increased, compared with those in the chemosensitive patients and BIU87 cells, respectively. However, the expression levels of
maspin were lower in the
cisplatin-resistant tissue and cells, and was enhanced by
IGFBP-2 inhibition.
Cisplatin (3 μM) caused marked proliferation inhibition, cell cycle arrest and apoptosis of the BIU87-CisR cells, the effect of which was enhanced by
IGFBP-2 silencing. Overexpression of
maspin also improved the sensitivity of the BIU87-CisR cells to
cisplatin. In conclusion, inhibition of
IGFBP-2 improved the sensitivity of
bladder cancer cells to
cisplatin by elevating the expression of
maspin.