资源类型:
期刊
WOS体系:
Article
Pubmed体系:
Journal Article
收录情况:
◇ SCIE
文章类型:
论著
机构:
[1]Afliated Cancer Hospital & Institute of Guangzhou Medical University, No.78 Hengzhigang Road, Guangzhou 510095, Guangdong, China
[2]Department of Clinical Laboratory, Sun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Guangzhou, China
[3]Department of Oncology, The Fifth Afliated Hospital, Guangzhou Medical University, Guangzhou, China
[4]Department of Laboratory, Guangzhou Women and Children’s Medical Centre, Guangzhou Medical University, Guangzhou, China
[5]Laboratory of Oncology Science and Molecular Biology, ShunDe Hospital of Guangzhou University of Chinese Medicine, No.12 Jinsha Avenue, Shunde District, Foshan 528333, Guangdong, China.
ISSN:
1756-9966
关键词:
Gastric carcinoma
Metastasis
lncRNA
SGO1-AS1
TGFβ
ZEB1
摘要:
Although thousands of long noncoding RNAs (lncRNAs) have been annotated, only a few lncRNAs have been characterized functionally. In this study, we aimed to identify novel lncRNAs involved in the progression of gastric carcinoma (GC) and explore their regulatory mechanisms and clinical significance in GC.A lncRNA expression microarray was used to identify differential lncRNA expression profiles between paired GCs and adjacent normal mucosal tissues. Using the above method, the lncRNA SGO1-AS1 was selected for further study. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) and in situ hybridization (ISH) were performed to detect SGO1-AS1 expression in GC tissues. Gain-of-function and loss-of-function analyses were performed to investigate the functions of SGO1-AS1 and its upstream and downstream regulatory mechanisms in vitro and in vivo.SGO1-AS1 was downregulated in gastric carcinoma tissues compared to adjacent normal tissues, and its downregulation was positively correlated with advanced clinical stage, metastasis status and poor patient prognosis. The functional experiments revealed that SGO1-AS1 inhibited GC cell invasion and metastasis in vitro and in vivo. Mechanistically, SGO1-AS1 facilitated TGFB1/2 mRNA decay by competitively binding the PTBP1 protein, resulting in reduced TGFβ production and, thus, preventing the epithelial-to-mesenchymal transition (EMT) and metastasis. In addition, in turn, TGFβ inhibited SGO1-AS1 transcription by inducing ZEB1. Thus, SGO1-AS1 and TGFβ form a double-negative feedback loop via ZEB1 to regulate the EMT and metastasis.SGO1-AS1 functions as an endogenous inhibitor of the TGFβ pathway and suppresses gastric carcinoma metastasis, indicating a novel potential target for GC treatment.© 2021. The Author(s).
基金:
National Natural Science Foundation of
China (No. 81972771, No. 81672452 and No. 81472625), National Natural
Science Foundation of Guangdong Province (No. 2018B0303110015 and
No. 2018A0303130314) and Guangdong Medical Research Foundation (No.
B2018283).
WOS:
WOS:000712588900001
PubmedID:
34706749
中科院(CAS)分区:
出版当年[2020]版:
大类
|
2 区
医学
小类
|
2 区
肿瘤学
最新[2025]版:
大类
|
1 区
医学
小类
|
1 区
肿瘤学
影响因子:
11.4
最新[2023版]
11.4
最新五年平均
7.068
出版当年[2019版]
6.53
出版当年五年平均
5.646
出版前一年[2018版]
11.161
出版后一年[2020版]
第一作者:
Huang Donglan
第一作者机构:
[1]Afliated Cancer Hospital & Institute of Guangzhou Medical University, No.78 Hengzhigang Road, Guangzhou 510095, Guangdong, China
共同第一作者:
Zhang Ke
通讯作者:
Gu Yixue;Xu Jianhua;Deng Min
推荐引用方式(GB/T 7714):
Huang Donglan,Zhang Ke,Zheng Wenying,et al.Long noncoding RNA SGO1-AS1 inactivates TGFβ signaling by facilitating TGFB1/2 mRNA decay and inhibits gastric carcinoma metastasis.[J].JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH.2021,40(1):doi:10.1186/s13046-021-02140-0.
APA:
Huang Donglan,Zhang Ke,Zheng Wenying,Zhang Ruixin,Chen Jiale...&Deng Min.(2021).Long noncoding RNA SGO1-AS1 inactivates TGFβ signaling by facilitating TGFB1/2 mRNA decay and inhibits gastric carcinoma metastasis..JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH,40,(1)
MLA:
Huang Donglan,et al."Long noncoding RNA SGO1-AS1 inactivates TGFβ signaling by facilitating TGFB1/2 mRNA decay and inhibits gastric carcinoma metastasis.".JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH 40..1(2021)