Evidence map›Paper›PMID 30607139›Full record

ArticleCancer cell international2018

Speckle-type POZ protein functions as a tumor suppressor in non-small cell lung cancer due to DNA methylation.

Sumei Yao, Xinming Chen, Jinliang Chen, Yangbo Guan, Yifei Liu, Jianrong Chen, Xuedong Lv

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 27% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.

  1. Pooled it
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  12. SPOP and cancer: a systematic review.American journal of cancer research · 2020
    Review
  13. Observational
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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.

Sumei Yao *1Department of Respiratory Medicine, The Second Affiliated Hospital of Nantong University, 6 Haierxiang North Road, Nantong, 226001 Jiangsu People's Republic of China.
Xinming Chen *2Department of Thoracic Surgery, Affiliated Hospital of Nantong University, Nantong, 226001 China.
Jinliang Chen *1Department of Respiratory Medicine, The Second Affiliated Hospital of Nantong University, 6 Haierxiang North Road, Nantong, 226001 Jiangsu People's Republic of China.
Yangbo Guan3Department of Urology, Affiliated Hospital of Nantong University, Nantong, 226001 China.
Yifei Liu3Department of Urology, Affiliated Hospital of Nantong University, Nantong, 226001 China.
Jianrong Chen1Department of Respiratory Medicine, The Second Affiliated Hospital of Nantong University, 6 Haierxiang North Road, Nantong, 226001 Jiangsu People's Republic of China.
Xuedong Lv1Department of Respiratory Medicine, The Second Affiliated Hospital of Nantong University, 6 Haierxiang North Road, Nantong, 226001 Jiangsu People's Republic of China.
Affiliated Hospital of Nantong University · CNSecond Affiliated Hospital of Nantong UniversityNantong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTumor suppressor epigenetic silencing plays an important role in non-small cell lung cancer (NSCLC) development and progression. Previously, the expression of speckle-type POZ protein (SPOP) has been found to be significantly inhibited in NSCLC. Our research aimed to investigate the molecular mechanisms, clinical significance and epigenetic alteration of SPOP in NSCLC. MATERIALS AND

methodsBisulfite sequencing PCR and methylation-specific PCR were performed to test gene methylation. Chromatin immunoprecipitation (ChIP) was performed to detect transcription factor C/EBPα combinations and the promoter of the SPOP gene. Furthermore, we evaluated the effects of C/EBPα siRNA on SPOP expression, tumor cell migration and proliferation via MTT and Transwell assays in vitro and tumor growth in vivo. The relationship between the methylation status of the SPOP gene and clinicopathologic characteristics was investigated.

resultsHypermethylation was found in the CpG island of the SPOP gene promoter in NSCLC tissues, and this methylation was found to be correlated with SPOP expression. SPOP promoter methylation was associated with the pathology grade. The transcriptional activities were significantly inhibited by the hypermethylation of specific CpG sites within the SPOP gene promoter, while 5-aza-2'-deoxycytidine significantly increased SPOP gene expression. C/EBPα also played a key role in SPOP regulation. Five C/EBPα binding sites in the CpG island of the SPOP gene promoter were identified by ChIP. Inhibition of C/EBPα significantly reduced SPOP expression. SPOP mediated the C/EBPα-regulated suppression of invasion, migration and proliferation in vitro and tumor growth in vivo.

conclusionsSPOP function and expression in NSCLS were regulated by DNA methylation and C/EBPα transcriptional regulation combination effects, indicating that the SPOP promoter methylation status could be utilized as an epigenetic biomarker and that the C/EBPα-SPOP signaling pathway could be a potential therapeutic target in NSCLC.

Indexed as

C/EBPαDNA methylationNSCLCSPOPTranscriptional regulation

Identifiers

PMID30607139
PMCPMC6304003
OpenAlexW2906137701

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LicenceCC BY
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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.