题名 | FAM83A antisense RNA 1 (FAM83A-AS1) silencing impairs cell proliferation and induces autophagy via MET-AMPKalpha signaling in lung adenocarcinoma |
作者 | |
通讯作者 | Chen, Guoan |
发表日期 | 2022-05-02
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DOI | |
发表期刊 | |
ISSN | 2165-5979
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EISSN | 2165-5987
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卷号 | 13期号:5 |
摘要 | Studies demonstrate that long non-coding RNAs (lncRNAs) play vital roles in cancer progression. However, the expression pattern and molecular mechanisms of lncRNA FAM83A-AS1 in lung cancer remain largely unclear. Here, we analyzed FAM83A-AS1 expression in lung cancer tissues from three RNA-sequencing (RNA-Seq) datasets and validated these results using quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) in an independent set of lung adenocarcinoma. Cell proliferation, migration, invasion, and autophagy were analyzed after knockdown FAM83A-AS1 with siRNAs. The underlying molecular mechanisms of FAM83A-AS1 were performed by Western blot, qRT-PCR, and RNA-seq analysis. We found that FAM83A-AS1 was up-regulated in lung cancer and elevated expression was associated with poor patient survival. These results were confirmed using RT-PCR in an independent set of lung cancer. Functional study indicated that FAM83A-AS1 knockdown reduced cell proliferation, migration, invasion, and colony formation in cancer cells. FAM83A-AS1 silencing induced autophagy and cell cycle arrest at G2. Mechanistically, serval oncogenic proteins such as EGFR, MET, PI3K, and K-RAS were decreased upon FAM83A-AS1 silencing, while phosphor AMPK alpha and ULK1 were increased. Based on the above results, we believe that FAM83A-AS1 may have potential as a diagnosis/prognosis marker and its oncogenic role and autophagy regulation may be through MET-AMPK alpha signaling, which could lead to potential targeting for lung cancer therapy. |
关键词 | |
相关链接 | [来源记录] |
收录类别 | |
语种 | 英语
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学校署名 | 第一
; 通讯
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资助项目 | Shenzhen Municipal Science and Technology Innovation Commission Foundation[2021-255]
; National Natural Science Foundation of China (NSFC)[32070625]
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WOS研究方向 | Biotechnology & Applied Microbiology
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WOS类目 | Biotechnology & Applied Microbiology
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WOS记录号 | WOS:000804154400001
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出版者 | |
来源库 | Web of Science
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引用统计 |
被引频次[WOS]:11
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成果类型 | 期刊论文 |
条目标识符 | http://sustech.caswiz.com/handle/2SGJ60CL/335797 |
专题 | 南方科技大学医学院 生命科学学院 南方科技大学医学院_人类细胞生物和遗传学系 |
作者单位 | 1.Southern Univ Sci & Technol, Sch Med, Shenzhen, Guangdong, Peoples R China 2.Southern Univ Sci & Technol, Sch Life Sci, Shenzhen, Guangdong, Peoples R China 3.Univ Michigan, Dept Surg, Med Sch, Ann Arbor, MI 48109 USA 4.Xinjiang Med Univ, Basic Med Coll, Dept Histol & Embryol, Urumqi, Peoples R China |
第一作者单位 | 南方科技大学医学院 |
通讯作者单位 | 南方科技大学医学院 |
第一作者的第一单位 | 南方科技大学医学院 |
推荐引用方式 GB/T 7714 |
Zhao, Huijie,Wang, Yinghan,Wu, Xing,et al. FAM83A antisense RNA 1 (FAM83A-AS1) silencing impairs cell proliferation and induces autophagy via MET-AMPKalpha signaling in lung adenocarcinoma[J]. Bioengineered,2022,13(5).
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APA |
Zhao, Huijie.,Wang, Yinghan.,Wu, Xing.,Zeng, Xaofei.,Lin, Baoyue.,...&Chen, Guoan.(2022).FAM83A antisense RNA 1 (FAM83A-AS1) silencing impairs cell proliferation and induces autophagy via MET-AMPKalpha signaling in lung adenocarcinoma.Bioengineered,13(5).
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MLA |
Zhao, Huijie,et al."FAM83A antisense RNA 1 (FAM83A-AS1) silencing impairs cell proliferation and induces autophagy via MET-AMPKalpha signaling in lung adenocarcinoma".Bioengineered 13.5(2022).
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