Adapting New Ways to Escape Attacks by Anti-Cancer Drugs: Epigenetic Changes and Alternative Splicing

The efficacy of cancer chemotherapy is often affected by the emergence of resistant cancer cells. While biochemical and pharmacological mechanisms have been proposed to explain chemoresistance, the genes involved in this process have not been fully identified. We previously used genomic DNA microarrays and quantitative RTPCR to identify the genes associated with resistance to chemotherapeutic drugs, particularly to the genotoxic agent cisplatin. Notably, knockdown of the cisplatin resistance (CPR) genes that we identified was shown to reduce chemoresistance and to suppress the growth of tumor xenographs in cisplatin-treated mice, indicating that the newly-identified CPR genes may represent potential therapy candidates to limit chemoresistance and to improve the efficacy of anticancer drugs. In addition to genetic mutations, researchers have found that epigenetic changes and alternative splicing of specific genes may also allow cancer cells to become resistant to chemotherapeutic drugs. In this short review, the author presents an overview of the latest findings in this field, with an emphasis on the adaptive responses of cancer cells to anticancer drugs.

並列關鍵字

alternative splicing ； cisplatin ； chemoresistance ； DNA microarray ； epigenetic modifications

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