Evidence map›Paper›PMID 30293090›Full record

ArticleCellular and molecular life sciences : CMLS2018

Long non-coding RNA AFAP1-AS1 plays an oncogenic role in promoting cell migration in non-small cell lung cancer.

Juan He, Ke Wu, Chenglin Guo, Jian-Kang Zhou, Wenchen Pu, Yulan Deng, Yuanli Zuo, Yun Zhao, Lunxu Liu, Yu-Quan Wei and 1 more

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. Pooled it
  2. Functional, Pharmacogenomic, and Immune Landscapes of Long Non-Coding RNAs in Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  13. Aberrant methylation-mediated downregulation of lncRNAJournal of biological research (Thessalonike, Greece) · 2020
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 1 institution in 1 country.

Juan HeDepartment of Thoracic Surgery, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University and Collaborative Innovation Center of Biotherapy, Renmin South Road, Section 3-17, Chengdu, 610041, China.
Ke WuDepartment of Thoracic Surgery, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University and Collaborative Innovation Center of Biotherapy, Renmin South Road, Section 3-17, Chengdu, 610041, China.
Chenglin GuoDepartment of Thoracic Surgery, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University and Collaborative Innovation Center of Biotherapy, Renmin South Road, Section 3-17, Chengdu, 610041, China.
Jian-Kang ZhouDepartment of Thoracic Surgery, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University and Collaborative Innovation Center of Biotherapy, Renmin South Road, Section 3-17, Chengdu, 610041, China.
Wenchen PuDepartment of Thoracic Surgery, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University and Collaborative Innovation Center of Biotherapy, Renmin South Road, Section 3-17, Chengdu, 610041, China.
Yulan DengDepartment of Thoracic Surgery, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University and Collaborative Innovation Center of Biotherapy, Renmin South Road, Section 3-17, Chengdu, 610041, China.
Yuanli ZuoCollege of Life Sciences, Sichuan University, Chengdu, 610064, China.
Yun ZhaoCollege of Life Sciences, Sichuan University, Chengdu, 610064, China.
Lunxu LiuDepartment of Thoracic Surgery, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University and Collaborative Innovation Center of Biotherapy, Renmin South Road, Section 3-17, Chengdu, 610041, China.
Yu-Quan WeiDepartment of Thoracic Surgery, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University and Collaborative Innovation Center of Biotherapy, Renmin South Road, Section 3-17, Chengdu, 610041, China.
Yong PengDepartment of Thoracic Surgery, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University and Collaborative Innovation Center of Biotherapy, Renmin South Road, Section 3-17, Chengdu, 610041, China. yongpeng@scu.edu.cn.ORCID http://orcid.org/0000-0002-1181-3467
Sichuan University · CN

Funding

National Key R&D Program of China 2016YFA0502204National Key R&D Program of China 2017YFA0504304National Natural Science Foundation of China 81572739National Natural Science Foundation of China 81772960
6 · The paper itself

Abstract

Long non-coding RNA (lncRNA) plays an important role in tumor progression and metastasis. Emerging evidence indicates that lncRNA actin filament-associated protein 1-antisense RNA 1 (AFAP1-AS1) is dysregulated in certain tumors. However, the function of AFAP1-AS1 in non-small cell lung cancer (NSCLC) remains elusive. In this study, we conducted global lncRNA profiling and identified that AFAP1-AS1 is significantly upregulated in NSCLC, suggesting that AFAP1-AS1 may be important for lung cancer development. For the first time, the transcription initiation and termination sites of AFAP1-AS1 were identified by rapid amplification of cDNA ends technology, and the sequencing data indicated that AFAP1-AS1 in lung cancer cells is a novel transcript variant. Through gain- and loss-of-function studies, AFAP1-AS1 was demonstrated to promote cell migration and invasion. Mechanistically, AFAP1-AS1 functions through positively regulating the expression of AFAP1 protein. On the other hand, the expression of lncRNA AFAP1-AS1 negatively correlates with CpG methylation status of its gene promoter, identified in both lung cancer cells and patient tissues, and treatment with DNA methyltransferase inhibitor decitabine significantly activates AFAP1-AS1 expression, strongly supporting that AFAP1-AS1 expression is tightly regulated by DNA methylation. Taken together, this study demonstrates that AFAP1-AS1 acts as an oncogene in NSCLC to promote cell migration partly by upregulating AFAP1 expression, while its own expression is controlled by DNA methylation, and highlights its diagnostic and therapeutic values for NSCLC patients.

Indexed as

Cell MovementGene Expression Regulation, NeoplasticCarcinoma, Non-Small-Cell LungCell Line, TumorDNA MethylationHumansLung NeoplasmsMicrofilament ProteinsNeoplasm InvasivenessRNA, Long NoncodingUp-RegulationAFAP1-AS1 long noncoding RNA, humanAFAP1 protein, humanMicrofilament ProteinsRNA, Long NoncodingAFAP1AFAP1-AS1Cell invasionCell migrationDNA methylationLung cancer

Identifiers

PMID30293090
PMCPMC11105532
OpenAlexW2894735066

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.