题名 | Long noncoding RNA MALAT1 regulates autophagy associated chemoresistance via miR-23b-3p sequestration in gastric cancer |
作者 | |
发表日期 | 2017-11-21 |
发表期刊 | MOLECULAR CANCER 影响因子和分区 |
语种 | 英语 |
原始文献类型 | Article |
关键词 | lncRNA MALAT1 Gastric cancer Chemoresistance Autophagy |
其他关键词 | COMPETING ENDOGENOUS RNA ; MULTIDRUG-RESISTANCE ; CELLS ; EXPRESSION ; SURVIVAL ; PROLIFERATION ; METASTASIS ; INCREASES ; CARCINOMA ; TARGET |
摘要 | Background: Chemoresistance has long been recognized as a major obstacle in cancer therapy. Clarifying the underlying mechanism of chemoresistance would result in novel strategies to improve patient's response to chemotherapeutics. Methods: lncRNA expression levels in gastric cancer (GC) cells was detected by quantitative real-time PCR (qPCR). MALAT1 shRNAs and overexpression vector were transfected into GC cells to down-regulate or up-regulate MALAT1 expression. In vitro and in vivo assays were performed to investigate the functional role of MALAT1 in autophagy associated chemoresistance. Results: We showed that chemoresistant GC cells had higher levels of MALAT1 and increased autophagy compared with parental cells. Silencing of MALAT1 inhibited chemo-induced autophagy, whereas MALAT1 promoted autophagy in gastric cancer cells. Knockdown of MALAT1 sensitized GC cells to chemotherapeutics. MALAT1 acts as a competing endogenous RNA for miR-23b-3p and attenuates the inhibitory effect of miR-23b-3p on ATG12, leading to chemo-induced autophagy and chemoresistance in GC cells. Conclusions: Taken together, our study revealed a novel mechanism of lncRNA-regulated autophagy-related chemoresistance in GC, casting new lights on the understanding of chemoresistance. |
资助项目 | National Nature Science Foundation of ChinaNational Natural Science Foundation of China (NSFC) [81702388]; Zhejiang province key science and technology innovation team [2013TD13]; Institute of Gastroenterology, Zhejiang University (IGZJU); Wenzhou Science and Technology Bureau [Y20160426] |
出版者 | BMC |
出版地 | LONDON |
ISSN | 1476-4598 |
EISSN | 1476-4598 |
卷号 | 16期号:1页码:174 |
DOI | 10.1186/s12943-017-0743-3 |
页数 | 12 |
WOS类目 | Biochemistry & Molecular Biology ; Oncology |
WOS研究方向 | Biochemistry & Molecular Biology ; Oncology |
WOS记录号 | WOS:000415986700001 |
收录类别 | SCIE ; PUBMED ; SCOPUS |
URL | 查看原文 |
PubMed ID | 29162158 |
PMC记录号 | PMC5699172 |
SCOPUSEID | 2-s2.0-85034628721 |
通讯作者地址 | [Yanfan, Chen]Department of radiology,Wenzhou No.3 Clinical Institute of Wenzhou Medical University,Wenzhou People's Hospital,No. 57 Canghou Street,,Wenzhou, Zhejiang,325000,China |
Scopus学科分类 | Molecular Medicine;Oncology;Cancer Research |
TOP期刊 | TOP期刊 |
引用统计 | |
文献类型 | 期刊论文 |
条目标识符 | https://kms.wmu.edu.cn/handle/3ETUA0LF/15492 |
专题 | 温州医科大学 |
通讯作者 | Yanfan, Chen |
作者单位 | 1.The third Clinical Institute Affiliated to Wenzhou Medical University,Wenzhou People's Hospital,Department of General Surgery,Wenzhou, Zhejiang,China; 2.The third Clinical Institute Affiliated to Wenzhou Medical University,Wenzhou People's Hospital,Department of Gastroenterology,Wenzhou, Zhejiang,China; 3.Zhejiang University(IGZJU),Institute of Gastroenterology,Hangzhou, Zhejiang,China; 4.Wenzhou No.3 Clinical Institute of Wenzhou Medical University,Wenzhou People's Hospital,Department of radiology,No. 57 Canghou Street,Wenzhou, Zhejiang,325000,China |
第一作者单位 | 温州医科大学 |
通讯作者单位 | 温州医科大学 |
第一作者的第一单位 | 温州医科大学 |
推荐引用方式 GB/T 7714 | YiRen, Hu,YingCong, Yu,Sunwu, You,et al. Long noncoding RNA MALAT1 regulates autophagy associated chemoresistance via miR-23b-3p sequestration in gastric cancer[J]. MOLECULAR CANCER,2017,16(1):174. |
APA | YiRen, Hu., YingCong, Yu., Sunwu, You., Keqin, Li., Xiaochun, Tong., ... & Yanfan, Chen. (2017). Long noncoding RNA MALAT1 regulates autophagy associated chemoresistance via miR-23b-3p sequestration in gastric cancer. MOLECULAR CANCER, 16(1), 174. |
MLA | YiRen, Hu,et al."Long noncoding RNA MALAT1 regulates autophagy associated chemoresistance via miR-23b-3p sequestration in gastric cancer".MOLECULAR CANCER 16.1(2017):174. |
条目包含的文件 | 条目无相关文件。 |
除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。
修改评论