{"title":"卵巢癌细胞顺铂耐药的MicroRNA-mRNA功能对。","authors":"Mei Liu, Xin Zhang, Chen-Fei Hu, Qing Xu, Hong-Xia Zhu, Ning-Zhi Xu","doi":"10.5732/cjc.013.10136","DOIUrl":null,"url":null,"abstract":"<p><p>Ovarian cancer is the leading cause of death in women worldwide. Cisplatin is the core of first-line chemotherapy for patients with advanced ovarian cancer. Many patients eventually become resistant to cisplatin, diminishing its therapeutic effect. MicroRNAs (miRNAs) have critical functions in diverse biological processes. Using miRNA profiling and polymerase chain reaction validation, we identified a panel of differentially expressed miRNAs and their potential targets in cisplatin-resistant SKOV3/DDP ovarian cancer cells relative to cisplatin-sensitive SKOV3 parental cells. More specifically, our results revealed significant changes in the expression of 13 of 663 miRNAs analyzed, including 11 that were up-regulated and 2 that were down-regulated in SKOV3/DDP cells with or without cisplatin treatment compared with SKOV3 cells with or without cisplatin treatment. miRNA array and mRNA array data were further analyzed using Ingenuity Pathway Analysis software. Bioinformatics analysis suggests that the genes ANKRD17, SMC1A, SUMO1, GTF2H1, and TP73, which are involved in DNA damage signaling pathways, are potential targets of miRNAs in promoting cisplatin resistance. This study highlights candidate miRNA-mRNA interactions that may contribute to cisplatin resistance in ovarian cancer. </p>","PeriodicalId":10034,"journal":{"name":"癌症","volume":"33 6","pages":"285-94"},"PeriodicalIF":0.0000,"publicationDate":"2014-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/0a/d0/cjc-33-06-285.PMC4059866.pdf","citationCount":"16","resultStr":"{\"title\":\"MicroRNA-mRNA functional pairs for cisplatin resistance in ovarian cancer cells.\",\"authors\":\"Mei Liu, Xin Zhang, Chen-Fei Hu, Qing Xu, Hong-Xia Zhu, Ning-Zhi Xu\",\"doi\":\"10.5732/cjc.013.10136\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Ovarian cancer is the leading cause of death in women worldwide. Cisplatin is the core of first-line chemotherapy for patients with advanced ovarian cancer. Many patients eventually become resistant to cisplatin, diminishing its therapeutic effect. MicroRNAs (miRNAs) have critical functions in diverse biological processes. Using miRNA profiling and polymerase chain reaction validation, we identified a panel of differentially expressed miRNAs and their potential targets in cisplatin-resistant SKOV3/DDP ovarian cancer cells relative to cisplatin-sensitive SKOV3 parental cells. More specifically, our results revealed significant changes in the expression of 13 of 663 miRNAs analyzed, including 11 that were up-regulated and 2 that were down-regulated in SKOV3/DDP cells with or without cisplatin treatment compared with SKOV3 cells with or without cisplatin treatment. miRNA array and mRNA array data were further analyzed using Ingenuity Pathway Analysis software. Bioinformatics analysis suggests that the genes ANKRD17, SMC1A, SUMO1, GTF2H1, and TP73, which are involved in DNA damage signaling pathways, are potential targets of miRNAs in promoting cisplatin resistance. This study highlights candidate miRNA-mRNA interactions that may contribute to cisplatin resistance in ovarian cancer. </p>\",\"PeriodicalId\":10034,\"journal\":{\"name\":\"癌症\",\"volume\":\"33 6\",\"pages\":\"285-94\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2014-06-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/0a/d0/cjc-33-06-285.PMC4059866.pdf\",\"citationCount\":\"16\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"癌症\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.5732/cjc.013.10136\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2014/2/28 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q\",\"JCRName\":\"Medicine\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"癌症","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.5732/cjc.013.10136","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2014/2/28 0:00:00","PubModel":"Epub","JCR":"Q","JCRName":"Medicine","Score":null,"Total":0}
MicroRNA-mRNA functional pairs for cisplatin resistance in ovarian cancer cells.
Ovarian cancer is the leading cause of death in women worldwide. Cisplatin is the core of first-line chemotherapy for patients with advanced ovarian cancer. Many patients eventually become resistant to cisplatin, diminishing its therapeutic effect. MicroRNAs (miRNAs) have critical functions in diverse biological processes. Using miRNA profiling and polymerase chain reaction validation, we identified a panel of differentially expressed miRNAs and their potential targets in cisplatin-resistant SKOV3/DDP ovarian cancer cells relative to cisplatin-sensitive SKOV3 parental cells. More specifically, our results revealed significant changes in the expression of 13 of 663 miRNAs analyzed, including 11 that were up-regulated and 2 that were down-regulated in SKOV3/DDP cells with or without cisplatin treatment compared with SKOV3 cells with or without cisplatin treatment. miRNA array and mRNA array data were further analyzed using Ingenuity Pathway Analysis software. Bioinformatics analysis suggests that the genes ANKRD17, SMC1A, SUMO1, GTF2H1, and TP73, which are involved in DNA damage signaling pathways, are potential targets of miRNAs in promoting cisplatin resistance. This study highlights candidate miRNA-mRNA interactions that may contribute to cisplatin resistance in ovarian cancer.
期刊介绍:
In July 2008, Landes Bioscience and Sun Yat-sen University Cancer Center began co-publishing the international, English-language version of AI ZHENG or the Chinese Journal of Cancer (CJC). CJC publishes original research, reviews, extra views, perspectives, supplements, and spotlights in all areas of cancer research. The primary criteria for publication in CJC are originality, outstanding scientific merit, and general interest. The Editorial Board is composed of members from around the world, who will strive to maintain the highest standards for excellence in order to generate a valuable resource for an international readership.