BACKGROUNDAt present, it has been known that cyclooxygenase-2 (COX-2) plays a crucial role in invasion, development and metastasis of non-small cell lung cancer (NSCLC). In order to explore whether the expression of COX-2 inhibits the occurrence and development of NSCLC, antisense vector of human COX-2 gene is transfected into COX-2 highly expressing NSCLC cell line H1299 and its effects on proliferation and sensitivity to cisplatin of H1299 are analysed.

METHODSH1299 cells were transfected with antisense vector of human COX-2 gene using LipoVecTM transfecting technique. Transfected cells were selected with Geneticin (G418). The COX-2 mRNA level was examined by using reverse polymerase chain reaction (RT-PCR). The COX-2 protein level was examined by Western Blot. The proliferative status and sensitivity to cisplatin of cells was measured by methabenzthiazuron (MTT) assay.

RESULTSRT-PCR showed a lower COX-2 mRNA level in transfected cells. The level of COX-2 protein was decreased apparently. The proliferative index of the transfected cells decreased significantly (P < 0.05). The IC50 value of cisplatin decreased remarkably in transfected cells (1.8mg/l) compared with that in H1299 cells without transfection (3.8mg/l) (P < 0.05).

CONCLUSIONSTransfection with antisense vector of human COX-2 gene can not only inhibit the proliferation of H1299 cells, but also increase the sensitivity to cisplatin of H1299 cells.