Evidence map›Paper›PMID 34715859›Full record

ArticleCancer cell international2021

LncRNA ASAP1-IT1 enhances cancer cell stemness via regulating miR-509-3p/YAP1 axis in NSCLC.

Yantao Liu, Yuping Yang, Lingli Zhang, Jiaqiang Lin, Bin Li, Min Yang, Honghui Li, Kangwu Chen, Wei Zhao

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.5field-weighted citation impact, top 44% 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

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3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 8 citations in OpenAlex.

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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

9 authors at 6 institutions in 2 countries.

Yantao LiuDepartment of Pharmacy, West China Second University Hospital, Sichuan University, Chengdu, China.
Yuping YangDepartment of Respiratory Medicine, The First Affiliated Hospital of Chengdu Medical College, Chengdu, China.
Lingli ZhangDepartment of Pharmacy, West China Second University Hospital, Sichuan University, Chengdu, China.
Jiaqiang LinSchool of Laboratory Medicine Chengdu Medical College, Chengdu, China.
Bin LiSchool of Laboratory Medicine Chengdu Medical College, Chengdu, China.
Min YangSchool of Laboratory Medicine Chengdu Medical College, Chengdu, China.
Honghui LiDepartment of Refractive Surgery, Chengdu Aier Eye Hospital, Chengdu, China.
Kangwu ChenDepartment of Orthopedic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, China. kangwuchen2008@hotmail.com.
Wei ZhaoSchool of Laboratory Medicine Chengdu Medical College, Chengdu, China. wzhao42@cityu.edu.hk.ORCID http://orcid.org/0000-0003-2421-7311
Chengdu Medical College · CNSichuan University · CNAnyang Eye Hospital · CNCity University of Hong Kong · HKFirst Affiliated Hospital of Chengdu Medical College · CNSoochow University · CN

Funding

National Natural Science Foundation of China 81602636
6 · The paper itself

Abstract

backgroundNon-small cell lung cancer (NSCLC) is a major cause of cancer-related death worldwide, and cancer stem cell is responsible for the poor clinical outcome of NSCLC. Previous reports indicated that long noncoding RNAs (lncRNAs) play important roles in maintaining cancer stemness, however, the underlying mechanisms remain unclear. This study investigates the role of ASAP1 Intronic Transcript 1 (ASAP1-IT1) in cancer cell stemness of NSCLC.

methodsThe expression of ASAP1-IT1, microRNA-509-3p (miR-509-3p) and apoptosis-/stemness-related genes was analyzed by qRT-PCR in NSCLC tissues, cancer cells and spheres of cancer stem cells. Knockdown of ASAP1-IT1 or overexpression of miR-509-3p in NSCLC cells by infection or transfection of respective plasmids. Sphere formation and colony formation were used to detect NSCLC stem cell-like properties and tumor growth in vitro. Luciferase reporter assays, RNA immunoprecitation (RIP) and qRT-PCR assays were used to analyze the interaction between lncRNA and miRNA. The expression of expression of regulated genes of ASAP1-IT1/miR-509-3p axis was evaluated by qRT-PCR and Western blot. The NSCLC xenograft mouse model was used to validate the role of ASAP1-IT1 in NSCLC stemness and tumor growth in vivo.

resultsASAP1-IT1 was up-regulated in NSCLC tissues, cancer cells, and in spheres of A549-derived cancer stem cells. Downregulation of ASAP1-IT1 or overexpression of miR-509-3p significantly decreased cell colony formation and stem cell-like properties of A549-dereived stem cells with decreased expression of stem cell biomarkers SOX2, CD34, and CD133, and suppressing the expression of cell growth-related genes, Cyclin A1, Cyclin B1, and PCNA. Furthermore, knockdown of ASAP1-IT1 or overexpression of miR-509-3p repressed tumor growth in nude mice via reducing expression of tumorigenic genes. ASAP1-IT1 was found to interact with miR-509-3p. Moreover, overexpression of ASAP1-IT1 blocked the inhibition by miR-509-3p on stem cell-like properties and cell growth of A549-dereived stem cells both in vitro and in vivo. Finally, the level of YAP1 was regulated by ASAP1-IT1 and miR-509-3p.

conclusionsYAP1-involved ASAP1-IT1/miR-509-3p axis promoted NSCLC progression by regulating cancer cell stemness, and targeting this signaling pathway could be is a promising therapeutic strategy to overcome NSCLC stemness.

Indexed as

ASAP-IT1Cancer stemnessmiR-509-3pNSCLCYAP1

Identifiers

PMID34715859
PMCPMC8555224
OpenAlexW3159943050

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