Long non-coding RNA-ATB induces trastuzumab resistance and aggravates the progression of gastric cancer by repressing miR- 200c via ZNF217 elevation  

作　　者：JIAZHUANG LI WEI ZHANG SHOUBAO GAO LI SUN QINGYANG TAI YING LIU 

机构地区：[1]The Second Department of Oncology,The Third Affiliated Hospital of Qiqihar Medical University,Qiqihar,China

出　　处：《BIOCELL》2023年第10期2313-2320,共8页生物细胞（英文）

基　　金：supported by grants from the Basic Scientific Research Fund for Heilongjiang Provincial Universities in 2018(2018-KYYWF-0105).

摘　　要：Background: Trastuzumab resistance accounts for chemotherapy failure in gastric cancer patients in clinicalpractice. The significance of long non-coding RNAs (lncRNAs) in the maintenance of drug resistance in gastriccancer has been already underlined. Method: This study aimed to identify the specific role of lncRNA-ATB in gastriccancer progression and trastuzumab resistance. The downstream miRs of lncRNA-ATB and target genes of miRs werepredicted by bioinformatics analysis and verified using dual luciferase reporter assay. Loss- and gain-function assayswere performed to explore the roles of lncRNA-ATB, miR-200c, and zinc-finger protein 217 (ZNF217) in the cellfunctions and trastuzumab resistance of a trastuzumab-resistant gastric cancer cell line (NCI-N87-TR). Result:LncRNA-ATB was upregulated, while miR-200c was downregulated. Depletion of lncRNA-ATB or miR-200celevation led to a decrease in malignant properties of NCI-N87-TR cells. LncRNA-ATB could negatively target miR-200c, which in turn inversely targeted and reduced the expression of ZNF217. Silencing of ZNF217 could inhibit cellviability and migration. Conclusion: lncRNA-ATB promoted the progression and trastuzumab resistance of gastriccancer by repressing miR-200c via ZNF217 upregulation.

关 键 词：Gastric cancer Long noncoding RNA-ATB MicroRNA 200c Zinc finger protein 217 Migration VIABILITY Trastuzumab resistance 

分 类 号：R73[医药卫生—肿瘤]