Evidence map›Paper›PMID 35500152›Full record

ArticleJournal of clinical laboratory analysis2022

Super enhancer-LncRNA SENCR promoted cisplatin resistance and growth of NSCLC through upregulating FLI1.

Qiang Shen, Huixin Zhou, Meijuan Zhang, Ruihao Wu, Liangxing Wang, Yumin Wang, Jie Chen

Open access · goldAbstract read
In one paragraph

Article in Journal of clinical laboratory analysis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

11 citing papers in PubMed, 18 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

7 authors at 3 institutions in 1 country.

Qiang ShenFirst People's Hospital of Linping District, Hangzhou, China.
Huixin ZhouDepartment of Laboratory Medicine, Key Laboratory of Clinical Laboratory Diagnosis and Translational Research of Zhejiang Province, Zhejiang, China.
Meijuan ZhangDepartment of Laboratory Medicine, Key Laboratory of Clinical Laboratory Diagnosis and Translational Research of Zhejiang Province, Zhejiang, China.
Ruihao WuDepartment of Laboratory Medicine, Key Laboratory of Clinical Laboratory Diagnosis and Translational Research of Zhejiang Province, Zhejiang, China.
Liangxing WangFirst People's Hospital of Linping District, Hangzhou, China.
Yumin WangDepartment of Respiratory, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.ORCID https://orcid.org/0000-0001-8243-3659
Jie ChenDepartment of Intensive Care Unit, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Blood Center of Zhejiang Province · CNHangzhou First People's Hospital · CNWenzhou Medical University · CN

Funding

National Natural Science Foundation of China 81672088the Wenzhou Science and Technology Bureau Y20180501the Zhejiang Research Center for Intelligent Diagnosis and Molecular Technology of Tumors JBZX- 202003Zhejiang Provincial Health Planning Commission 2021KY784
6 · The paper itself

Abstract

backgroundSuper enhancer-lncRNA smooth muscle and endothelial cell-enriched migration/differentiation-associated lncRNA (SENCR) were highly overexpressed in cisplatin-resistant A549/DDP cells, while the mechanism was unclear.

methodsSE-lncRNA SENCR and FLI1 mRNA expression in A549/DDP cell, LAD tissues were detected. SENCR knockdown of A549/DDP cell and SENCR overexpression of cisplatin-sensitive A549 cell were constructed. Experiments of cell-confirmed function of SENCR and the correlation between SENCR and FLI1 were validated.

resultsThe expression of SENCR and FLI1 mRNA in A549/DDP cell were both upregulated and mainly localized in the nucleus. Compared with DDP-sensitive tissues with disease relief, SENCR expression was higher in DDP-resistant tissues with disease progression from LAD. Knockdown of SENCR in A549/DDP reduced proliferation ability and cisplatin resistance, consistent with the decreased levels of proteins PCNA, MDMX, and P-gp. Besides, whatever without cisplatin or with 2 μg/ml cisplatin, knockdown of SENCR reduced the migration, invasion, and colony formation abilities of A549/DDP cell and promoted apoptosis. However, when SENCR was overexpressed in A549 cell, all above results were reversed. Mechanistically, FLI1 expression was reduced after knocking down SENCR, while overexpressing SENCR increased FLI1 expression.

conclusionSE-LncRNA SENCR was upregulated in A549/DDP, which could promote cisplatin resistance and growth of NSCLC cell through upregulating FLI1 expression.

Indexed as

Antineoplastic AgentsCarcinoma, Non-Small-Cell LungLung NeoplasmsRNA, Long NoncodingA549 CellsApoptosisCell ProliferationCisplatinDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHumansRNA, MessengerAntineoplastic AgentsCisplatinRNA, Long NoncodingRNA, Messengercisplatin resistancenon-small cell lung cancersmooth muscle and endothelial cell enriched migration/differentiation-associated lncRNAsuper enhancer-lncRNA

Identifiers

PMID35500152
PMCPMC9169188
OpenAlexW4225263784

What OpenQuestion holds

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Registered trials

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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.