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

IF 1.6 Q3 MEDICINE, RESEARCH & EXPERIMENTAL Current Therapeutic Research-clinical and Experimental Pub Date : 2023-01-01 DOI:10.1016/j.curtheres.2023.100700

Jing Chen M.D. , Ming-Yuan Zhu M.D. , Yan-Hua Huang M.D. , Yi-Ting Ling M.D. , Tian-Yuan Gu M.D. , Quan Zhou M.D. , Ming-Jian Fei M.D. , Zhong-Cheng Zhou M.D.

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Abstract

Background

Antisense transcript of the B-cell translocation gene 3 (ASBEL) is a highly conserved antisense 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 evaluated the expression of ASBEL and BTG3 in tumor tissues and cells using Western blotting and quantitative 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 invasion 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).

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B细胞转运基因非编码RNA反义转录3调控BTG3在胰腺导管腺癌肿瘤进展中的作用

背景B细胞易位基因3反义转录物（ASBEL）是一种高度保守的反义非编码RNA（ncRNA），参与多种生物学过程。然而，ASBEL在胰腺导管腺癌（PDAC）中的表达状态及其与BTG3表达和肿瘤细胞进展的相关性尚不完全清楚。目的通过细胞实验和动物实验证实ASBEL通过靶向BTG3在PDAC的肿瘤发生中起着至关重要的作用。方法采用Western印迹、定量聚合酶链反应、细胞计数试剂盒-8、流式细胞术和细胞转染等方法评价ASBEL在PDAC肿瘤发生中的调控作用。我们还使用Western印迹和定量实时聚合酶链反应评估了ASBEL和BTG3在肿瘤组织和细胞中的表达。最后，我们通过分别在AsPC-1或CFPAC-1细胞中沉默或过表达ASBEL基因来探索ASBEL在肿瘤发展中的作用，并使用ASBEL拮抗剂评估体内抗肿瘤活性。结果ASBEL在所有胰腺细胞系中均有表达。ASBEL在肿瘤组织中的表达水平高于癌旁组织。ASBEL抑制BTG3的表达，增强增殖和抑制凋亡，促进胰腺癌症细胞的迁移和侵袭。拮抗剂调节ASBEL在AsPC-1中的表达，并抑制异种移植小鼠模型中的肿瘤生长。结论ASBEL可能通过靶向BTG3在PDAC中发挥肿瘤促进因子的作用，可能成为PDAC治疗的重要生物标志物。（Curr Ther Res Clin Exp.2023；84:XXX–XXX）。

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来源期刊

Current Therapeutic Research-clinical and Experimental 医学-药学

CiteScore

3.50

自引率

0.00%

发文量

审稿时长

3 months

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