Evidence map›Paper›PMID 30737371›Full record

ArticleCell death & disease2019

miR-1260b, mediated by YY1, activates KIT signaling by targeting SOCS6 to regulate cell proliferation and apoptosis in NSCLC.

Yang Xia, Ke Wei, Feng-Ming Yang, Liu-Qing Hu, Chun-Feng Pan, Xiang-Long Pan, Wei-Bing Wu, Jun Wang, Wei Wen, Zhi-Cheng He and 4 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

31 citing papers in PubMed, 67 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 2 institutions in 1 country.

Yang XiaDepartment of Thoracic Surgery, the First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Ke WeiDepartment of Thoracic Surgery, the First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Feng-Ming YangDepartment of Oncology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Liu-Qing HuDepartment of Anesthesiology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Chun-Feng PanDepartment of Thoracic Surgery, the First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Xiang-Long PanDepartment of Thoracic Surgery, the First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Wei-Bing WuDepartment of Thoracic Surgery, the First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Jun WangDepartment of Thoracic Surgery, the First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Wei WenDepartment of Thoracic Surgery, the First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Zhi-Cheng HeDepartment of Thoracic Surgery, the First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Jing XuDepartment of Thoracic Surgery, the First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Xin-Feng XuDepartment of Thoracic Surgery, the First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Quan ZhuDepartment of Thoracic Surgery, the First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China. chest2006@163.com.
Liang ChenDepartment of Thoracic Surgery, the First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China. clbright0909@njmu.edu.cn.
Nanjing Medical University · CNJiangsu Province Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-small cell lung cancer (NSCLC) is one of the most common aggressive malignancies. miRNAs have been identified as important biomarkers and regulators of NSCLC. However, the functional contributions of miR-1260b to NSCLC cell proliferation and apoptosis have not been studied. In this study, miR-1260b was upregulated in NSCLC plasma, tissues, and cell lines, and its high expression was correlated with tumor size and progression. Functionally, miR-1260b overexpression promoted cell proliferation and cell cycle, conversely inhibited cell apoptosis and senescence. Mechanically, miR-1260b negatively regulated SOCS6 by directly binding to its 3'-UTR. Furthermore, miR-1260b-mediated suppression of SOCS6 activated KIT signaling. Moreover, YY1 was an upstream regulator of miR-1260b. This study is the first to illustrate that miR-1260b, mediated by YY1, activates KIT signaling by targeting SOCS6 to regulate NSCLC cell proliferation and apoptosis, and is a potential biomarker and therapeutic target for NSCLC. In sum, our work provides new insights into the molecular mechanisms of NSCLC involved in cell proliferation and apoptosis.

Indexed as

ApoptosisCarcinoma, Non-Small-Cell LungCell Line, TumorCell ProliferationHumansLung NeoplasmsMicroRNAsProto-Oncogene Proteins c-kitSignal TransductionSuppressor of Cytokine Signaling ProteinsTransfectionUp-RegulationYY1 Transcription FactorKIT protein, humanMicroRNAsMIRN1260 microRNA, humanProto-Oncogene Proteins c-kitSOCS6 protein, humanSuppressor of Cytokine Signaling ProteinsYY1 protein, humanYY1 Transcription Factor

Identifiers

PMID30737371
PMCPMC6368632
OpenAlexW2912440762

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.