Evidence map›Paper›PMID 31382188›Full record

ArticleMolecular therapy. Nucleic acids2019

LINC00472 Acts as a Tumor Suppressor in NSCLC through KLLN-Mediated p53-Signaling Pathway via MicroRNA-149-3p and MicroRNA-4270.

Aimei Zou, Xingli Liu, Zongjiong Mai, Junke Zhang, Zhuohuan Liu, Qilu Huang, Aibing Wu, Chenyu Zhou

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Molecular therapy. Nucleic acids, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

24 citing papers in PubMed, 36 citations in OpenAlex.

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  20. Gene expression profiling after LINC00472 overexpression in an NSCLC cell line1.Cancer biomarkers : section A of Disease markers · 2021
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 1 country.

Aimei ZouDepartment of Oncology, Shunde Hospital, Southern Medical University (The First People's Hospital of Shunde), Foshan 528308, P.R. China.
Xingli LiuDepartment of Oncology, Shunde Hospital, Southern Medical University (The First People's Hospital of Shunde), Foshan 528308, P.R. China.
Zongjiong MaiArea 7 of Tumor Chemotherapy Department, Central Hospital of Guangdong Nongken, Zhanjiang 524001, P.R. China.
Junke ZhangDepartment of Oncology, Shunde Hospital, Southern Medical University (The First People's Hospital of Shunde), Foshan 528308, P.R. China.
Zhuohuan LiuDepartment of Oncology, Shunde Hospital, Southern Medical University (The First People's Hospital of Shunde), Foshan 528308, P.R. China.
Qilu HuangDepartment of Oncology, Affiliated Hospital of Guangdong Medical University, Zhanjiang 524001, P.R. China.
Aibing WuDepartment of Oncology, Affiliated Hospital of Guangdong Medical University, Zhanjiang 524001, P.R. China. Electronic address: wab80106@163.com.
Chenyu ZhouDepartment of Oncology, Shunde Hospital, Southern Medical University (The First People's Hospital of Shunde), Foshan 528308, P.R. China. Electronic address: zhouchengyu1966@21cn.com.
The First People's Hospital of Shunde · CNGuangdong Medical College · CNCentral People's Hospital of Zhanjiang · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long non-coding RNAs and microRNAs (miRNAs) have been reported to participate in the progression of non-small-cell lung cancer (NSCLC). Long intergenic non-protein-coding RNA 472 (LINC00472), miR-149-3p, and miR-4270 were found to be involved in tumor activities, suggesting potential roles in NSCLC. Thus, this study aimed to examine the ability of LINC00472 to influence the progression of NSCLC with the involvement of miR-149-3p and miR-4270. Initially, differentially expressed long non-coding RNAs (lncRNAs), downstream regulatory miRNAs, and genes related to NSCLC were identified. Next, the interaction among LINC00472, miR-149-3p and miR-4270, and KLLN and the p53-signaling pathway was determined. The effect of LINC00472 on the expression of E-cadherin, N-cadherin, and Vimentin was examined through gain-of-function and loss-of-function experiments. Lastly, the effects of LINC00472 on NSCLC tumor growth were assessed in vivo. LINC00472 and KLLN were found to exhibit low levels, while miR-149-3p and miR-4270 were highly expressed in NSCLC. In addition, the overexpression of LINC00472 was observed to upregulate KLLN and activate the p53-signaling pathway, which ultimately inhibited the invasion, migration, and EMT of NSCLC cells via miR-149-3p and miR-4270, corresponding to decreased N-cadherin and Vimentin and increased E-cadherin. The overexpression of LINC00472 exerted an inhibitory effect on tumor growth in vivo. Taken together, the key evidence suggests that the overexpression of LINC00472 can downregulate miR-149-3p and miR-4270 to upregulate KLLN and activate the p53-signaling pathway, thus inhibiting the development of NSCLC. This study highlights the potential of LINC00472 as a promising therapeutic target for NSCLC treatment.

Indexed as

epithelial-mesenchymal transitioninvasionKLLNlong intergenic non-protein-coding RNA 472microRNA-149-3pmicroRNA-4270migrationnon-small-cell lung cancerp53-signaling pathway

Identifiers

PMID31382188
PMCPMC6676247
OpenAlexW2951334981

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.