作者: Mantang Qiu , Wenjia Xia , Rui Chen , Siwei Wang , Youtao Xu
DOI: 10.1158/0008-5472.CAN-17-2808
关键词: Cancer research 、 Transcription factor 、 Amplicon 、 Regulation of gene expression 、 Biology 、 Carcinogenesis 、 RNA 、 Adenocarcinoma 、 Copy-number variation 、 Circular RNA
摘要: Somatic copy number variations (CNV) may drive cancer progression through both coding and noncoding transcripts. However, transcripts resulting from CNV are largely unknown, especially for circular RNAs. By integrating bioinformatics analyses of alerted circRNAs focal in lung adenocarcinoma, we identify a proto-oncogenic RNA (circPRKCI) the 3q26.2 amplicon, one most frequent genomic aberrations multiple cancers. circPRKCI was overexpressed adenocarcinoma tissues, part due to amplification locus, promoted proliferation tumorigenesis adenocarcinoma. functioned as sponge miR-545 miR-589 abrogated their suppression protumorigenic transcription factor E2F7 Intratumor injection cholesterol-conjugated siRNA specifically targeting inhibited tumor growth patient-derived xenograft model. In summary, is crucial serve potential therapeutic target patients with adenocarcinoma.Significance: These findings reveal high expression drives tumorigenesis. Cancer Res; 78(11); 2839-51. ©2018 AACR.