Evidence map›Paper›PMID 33191397›Full record

ArticleCell death & disease2020

ZEB1-activated LINC01123 accelerates the malignancy in lung adenocarcinoma through NOTCH signaling pathway.

Miao Zhang, Yaguang Han, Yi Zheng, Yan Zhang, Xin Zhao, Zhenlin Gao, Xinyan Liu

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.1field-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

26 citing papers in PubMed, 37 citations in OpenAlex.

  1. Mechanistic insights into the lncRNA-Notch signaling axis in tumors.Frontiers in cell and developmental biology · 2026
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  15. ZEB1-activated Notch1 promotes circulating tumor cell migration and invasion in lung squamous cell carcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
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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 1 institution in 1 country.

Miao ZhangDepartment of Oncology, The NO.1 Hospital of Shijiazhuang in Hebei Province, 050010, Shijiazhuang, Hebei, China.
Yaguang HanDepartment of Oncology, The NO.1 Hospital of Shijiazhuang in Hebei Province, 050010, Shijiazhuang, Hebei, China.
Yi ZhengDepartment of Oncology, The NO.1 Hospital of Shijiazhuang in Hebei Province, 050010, Shijiazhuang, Hebei, China.
Yan ZhangDepartment of Oncology, The NO.1 Hospital of Shijiazhuang in Hebei Province, 050010, Shijiazhuang, Hebei, China. zhangyan201810@163.com.
Xin ZhaoDepartment of Oncology, The NO.1 Hospital of Shijiazhuang in Hebei Province, 050010, Shijiazhuang, Hebei, China.
Zhenlin GaoDepartment of Oncology, The NO.1 Hospital of Shijiazhuang in Hebei Province, 050010, Shijiazhuang, Hebei, China.
Xinyan LiuDepartment of Oncology, Hebei Provincial Thoracic Hospital, 050010, Shijiazhuang, Hebei, China.
First Hospital of Shijiazhuang · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Growing incidence of lung adenocarcinoma (LUAD) has been detected recently. Multiple long non-coding RNAs (lncRNAs) have been proven as tumor facilitators or inhibitors by extensive works. Present study concentrated on characterizing the potential role of LINC01123 in LUAD. We explored the differential expression of LINC01123 through qRT-PCR and found the amplification of LINC01123 in LUAD cell lines. It was ascertained that LINC01123 was definitely responsible for the malignant processes of LUAD cells. Further, we validated the ceRNA network of LINC01123/miR-449b-5p/NOTCH1 in LUAD via mechanical experiments. As a transcriptional factor related to epithelial mesenchymal transition (EMT), ZEB1 was responsible for the transcriptional activation of both LINC01123 and NOTCH1. The involvement of NOTCH signaling in LUAD was interrogated through evaluating functional changes after treating with FLI-06 (NOTCH pathway suppressor). It showed that FLI-06-caused NOTCH signaling inactivation suppressed malignant functions in LUAD cells. Additionally, LINC01123 facilitated NOTCH1-dependent NOTCH signaling activation. Rescue experiments probed the modulatory function of LINC01123/miR-449b-5p/NOTCH1 in LUAD cellular processes. Altogether, ZEB1-activated LINC01123 accelerates the malignancy in LUAD through miR-449b-5p/NOTCH1 axis-mediated NOTCH signaling pathway, while NOTCH1 boosts ZEB1 in return. These observations suggest the huge potential of LINC01123 as a new target for LUAD therapy.

Indexed as

Adenocarcinoma of LungCell Growth ProcessesHumansLung NeoplasmsNeoplastic Stem CellsReceptor, Notch1RNA, Long NoncodingSignal TransductionTransfectionZinc Finger E-box-Binding Homeobox 1long non-coding RNA LINC01133, humanNOTCH1 protein, humanReceptor, Notch1RNA, Long NoncodingZEB1 protein, humanZinc Finger E-box-Binding Homeobox 1

Identifiers

PMID33191397
PMCPMC7667157
OpenAlexW3101744942

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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.