The Role of Noncoding RNA Antisense Transcript of the B-Cell Translocation Gene 3 Regulation of BTG3 in Pancreatic Ductal Adenocarcinoma Tumor Progression

被引:0
|
作者
Chen, Jing [1 ]
Zhu, Ming -Yuan [1 ]
Huang, Yan-Hua [1 ]
Ling, Yi-Ting [1 ]
Gu, Tian -Yuan [1 ]
Zhou, Quan [2 ]
Fei, Ming-Jian [2 ]
Zhou, Zhong-Cheng [1 ,3 ]
机构
[1] Jiaxing Univ, Dept Gen Surg, Affiliated Hosp 2, Zhejiang, Peoples R China
[2] Jiaxing Univ, Dept Pathol, Affiliated Hosp 2, Zhejiang, Peoples R China
[3] Jiaxing Univ, Dept Hepatobiliary Surg, Affiliated Hosp 2, 1517 Huancheng North Rd, Jiaxing 314000, Zhejiang, Peoples R China
关键词
ASBEL; Antagonist; Long chain noncoding RNA; Pancreatic ductal adenocarcinoma; RNA interference; COMPLEX;
D O I
10.1016/j.curtheres.2023.100700
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Background: Antisense transcript of the B-cell translocation gene 3 (ASBEL) is a highly conserved anti -sense non-coding RNA (ncRNA) and participates in a variety of biological processes. However, the ASBEL expression status in pancreatic ductal adenocarcinoma (PDAC) and its correlation with BTG3 expression and tumor cell progression were not completely clear.Objective: We conducted cell experiments and animal experiments to confirm that ASBEL plays a crucial role in the tumorigenesis of PDAC by targeting BTG3. Methods: ASBEL regulation in PDAC tumorigenesis was evaluated using Western blotting, quantitative polymerase chain reaction, Cell Counting Kit-8 assay, flow cytometry, and cell transfection. We also eval-uated the expression of ASBEL and BTG3 in tumor tissues and cells using Western blotting and quanti-tative real-time polymerase chain reaction. Finally, we explored the role of ASBEL in tumor development by silencing or overexpressing ASBEL gene in AsPC-1 or CFPAC-1 cells, respectively, and evaluated the antitumor activity in vivo using an ASBEL antagonist.Results: Our study revealed the expression of ASBEL in all pancreatic cell lines. The expression level of ASBEL in tumor tissues was found to be higher than that of paracarcinomatous tissues. ASBEL suppresses expression of BTG3, enhances proliferation and suppresses apoptosis, and promotes migration and inva-sion in pancreatic cancer cell. Antagonist regulates the expression of ASBEL in AsPC-1, and suppresses tumor growth in xenograft mouse model.Conclusions: Our results indicate that ASBEL may play a tumor-promoting factor in PDAC by targeting BTG3 and could be as an important biomarker for PDAC treatment. (Curr Ther Res Clin Exp. 2023; 84:XXX- XXX).& COPY; 2023 The Author(s). Published by Elsevier Inc. This is an open access article under the CC BY-NC-ND license ( http://creativecommons.org/licenses/by-nc-nd/4.0/ )
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页数:10
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