Abstract
Resistance to chemotherapeutic agents is the major reason for treatment failure of cancer chemotherapy. Some chemotherapeutic drugs induce the activation of NF-κB in cancer cells that results in their resistance to anticancer drugs. But the role of NF-κB in acquired resistance has not been well investigated. In this study, we transferred the “super-repressor” form of the NF-κB inhibitor by adenoviral vector (ad-IκBα) to human lung cancer cell lines with resistant to cisplatin (PC-14-DDP) and adriamycin (PC-14-ADR), and observed the sensitivity change. Electrophoretic mobility shift assay showed that ad-IκBα blocked the activation of NF-κB induced by cisplatin and adriamycin. Transduction with ad-IκBα restored the sensitivity of cisplatin and adriamycin resistant lung cancer cell lines (PC-14-DDP and PC-14-ADR) to a level compatible to the parental cell lines. Annexin-V analysis suggested that the enhancement of chemosensitivity was probably a result of the induction of apoptosis. These data demonstrated that ad-IκBα blockade of chemotherapeutic induced NF-κB activation increased apoptosis induction and the chemosensitivity of lung cancer cell lines with acquired resistance to cisplatin and adriamycin. Therefore, gene transfer of IκBα-SR seems to represent a new therapeutic strategy for the solution of low sensitivity and lung cancer resistance to anticancer drugs.
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