Circular RNA AKT3 upregulates PIK3R1 to enhance cisplatin resistance in gastric cancer via miR-198 suppression

• DOI: 10.1186/s12943-019-0969-3
• Publication Date: 2019-03-30T06:03:03Z
• Authors: Xiaoxu Huang; Zheng Li; Qiang Zhang; Weizhi Wang; Bowen Li; Lu Wang; Zhipeng Xu; Ailiang Zeng; Xing Zhang; Xuan Zhang; Zhongyuan He; Qiang Li; Guangli Sun; Sen Wang; Qing Li; Linjun Wang; Lu Zhang; Hao Xu; Zekuan Xu
• Keywords: Clonogenic assay; Circular RNA

Cisplatin (CDDP) treatment is one of the most predominant chemotherapeutic strategies for patients with gastric cancer (GC). A better understanding mechanisms CDDP resistance can greatly improve therapeutic efficacy in GC. Circular RNAs (circRNAs) are a class noncoding whose functions related to pathogenesis cancer, but, GC remains unknown. circAKT3 (hsa_circ_0000199, circRNA originating from exons 8, 9, 10, and 11 AKT3 gene) was identified by RNA sequencing verified quantitative reverse transcription PCR. The role assessed both vitro vivo. Luciferase reporter assay, biotin-coupled pull-down fluorescence situ hybridization (FISH) were conducted evaluate interaction between miR-198. Functional experiments measured western blotting, cytotoxicity clonogenic assay flow cytometry. expression higher CDDP-resistant tissues cells than CDDP-sensitive samples. upregulation receiving therapy significantly associated aggressive characteristics an independent risk factor disease-free survival (DFS). Our data indicated that promotes DNA damage repair inhibits apoptosis vivo vitro. Mechanistically, we could promote PIK3R1 sponging plays important CDDP. Thus, our results highlight potential as target therapy.