Overexpression of ILK promotes temozolomide resistance in glioma cells.

The present study aimed to investigate whether overexpression of integrin-linked kinase (ILK) affects drug resistance to temozolomide (TMZ) in glioma cells. To do this, a plasmid containing the ILK gene was transfected into the SHG‑44 human glioma cell line, and cells were subsequently cultured in the absence or presence of TMZ. The expression levels of ILK, multidrug resistance‑associated protein (MRP) and multi‑drug resistance protein (MDR) were assessed in these cells. Cell growth and apoptosis were measured by MTT and Hoechst staining, and flow cytometry, respectively. In addition, the expression levels of B‑cell lymphoma 2 (Bcl‑2) and Bcl‑2‑associated x protein (Bax), and caspase‑3 activity, were evaluated. The ILK‑overexpressing SHG‑44 cell was successfully constructed, and demonstrated increased expression levels of ILK, MDR and MRP compared with untransfected cells. Cell growth in the ILK+TMZ group was significantly greater, and the percentage of apoptotic cells in the ILK+TMZ group was significantly reduced, compared with the p enhanced green fluorescent protein (EGFP)‑C1+ TMZ empty vector control group. Expression levels of the anti‑apoptotic protein Bcl‑2 were significantly increased and those of the pro‑apoptotic protein Bax were significantly decreased (P<0.01) in the ILK+TMZ group compared with the pEGFP‑C1+TMZ group. In addition, the activity of caspase‑3 in ILK+TMZ group was significantly decreased compared with the pEGFP‑C1+TMZ group (P<0.01). Overexpression of ILK therefore promoted the proliferation of SHG‑44 human glioma cells, reduced apoptosis and reduced sensitivity to TMZ via decreasing the activity of caspase‑3.