ABSTRACT
Excision repair cross complementation group-1 (ERCC1) was reported to be responsible for drug resistance during cancer treatment. In this report, we first proved the existence of ERCC1 exon VIII alternative splicing in ovarian cancer cells. Further investigation showed that over-expressed exon VIII deficient ERCC1 variant failed to change the protein level of ERCC1 in cancer cells, but decreased the excision repair function of ERCC1 and enhanced sensitivity of cancer cells to cisplatin in a dose-dependent manner. The results indicate that ERCC1 exon VIII alternative splicing does exist in some ovarian cancer cell lines, and regulates cisplatin-resistance in ovarian cancer cells.
ACKNOWLEDGMENTS
We sincerely express our gratitude to Luguo Sun (Jilin University), Wen Xiong (Shenzhen Blood Center), and Xiuqing Wang (Ouhsc) for their helpful recommendations, and to Ruifang Huang in our group, who has provided us all the technical assistances we needed.