Evidence map›Paper›PMID 32307642›Full record

ArticlePathology oncology research : POR2020

Promoter Hypomethylation and Increased Expression of the Long Non-coding RNA LINC00152 Support Colorectal Carcinogenesis.

Orsolya Galamb, Alexandra Kalmár, Anna Sebestyén, Titanilla Dankó, Csilla Kriston, István Fűri, Péter Hollósi, István Csabai, Barnabás Wichmann, Tibor Krenács and 7 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Pathology oncology research : POR, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.0field-weighted citation impact, top 30% 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

9 citing papers in PubMed, 15 citations in OpenAlex.

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  7. Fibroma of tendon sheath is defined by a USP6 gene fusion-morphologic and molecular reappraisal of the entity.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2021
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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

17 authors at 2 institutions in 1 country.

Orsolya Galamb2nd Department of Internal Medicine, Semmelweis University, Szentkirályi str 46, 1088, Budapest, Hungary. udvardyne_galamb.orsolya@semmelweis-univ.hu.ORCID http://orcid.org/0000-0002-7042-5667
Alexandra Kalmár2nd Department of Internal Medicine, Semmelweis University, Szentkirályi str 46, 1088, Budapest, Hungary.ORCID http://orcid.org/0000-0002-3824-1534
Anna Sebestyén1st Department of Pathology and Experimental Cancer Research, Semmelweis University, Budapest, Hungary.ORCID http://orcid.org/0000-0001-8814-4794
Titanilla Dankó1st Department of Pathology and Experimental Cancer Research, Semmelweis University, Budapest, Hungary.ORCID http://orcid.org/0000-0002-7419-4560
Csilla Kriston1st Department of Pathology and Experimental Cancer Research, Semmelweis University, Budapest, Hungary.ORCID http://orcid.org/0000-0003-0815-0401
István Fűri2nd Department of Internal Medicine, Semmelweis University, Szentkirályi str 46, 1088, Budapest, Hungary.ORCID http://orcid.org/0000-0001-7096-3177
Péter Hollósi1st Department of Pathology and Experimental Cancer Research, Semmelweis University, Budapest, Hungary.ORCID http://orcid.org/0000-0003-0458-8748
István CsabaiDepartment of Physics of Complex Systems, Eötvös Loránd University, Budapest, Hungary.ORCID http://orcid.org/0000-0001-9232-9898
Barnabás Wichmann2nd Department of Internal Medicine, Semmelweis University, Szentkirályi str 46, 1088, Budapest, Hungary.ORCID http://orcid.org/0000-0002-2320-8459
Tibor Krenács1st Department of Pathology and Experimental Cancer Research, Semmelweis University, Budapest, Hungary.ORCID http://orcid.org/0000-0001-9164-065X
Barbara Kinga Barták2nd Department of Internal Medicine, Semmelweis University, Szentkirályi str 46, 1088, Budapest, Hungary.ORCID http://orcid.org/0000-0002-1285-6768
Zsófia Brigitta Nagy2nd Department of Internal Medicine, Semmelweis University, Szentkirályi str 46, 1088, Budapest, Hungary.ORCID http://orcid.org/0000-0002-6237-9568
Sára Zsigrai2nd Department of Internal Medicine, Semmelweis University, Szentkirályi str 46, 1088, Budapest, Hungary.ORCID http://orcid.org/0000-0002-6161-5637
Gábor Barna1st Department of Pathology and Experimental Cancer Research, Semmelweis University, Budapest, Hungary.ORCID http://orcid.org/0000-0003-1960-5061
Zsolt TulassayMTA-SE Molecular Medicine Research Group, Hungarian Academy of Sciences and Semmelweis University, Budapest, Hungary.ORCID http://orcid.org/0000-0003-2452-6640
Péter Igaz2nd Department of Internal Medicine, Semmelweis University, Szentkirályi str 46, 1088, Budapest, Hungary.ORCID http://orcid.org/0000-0003-2192-554X
Béla Molnár2nd Department of Internal Medicine, Semmelweis University, Szentkirályi str 46, 1088, Budapest, Hungary.ORCID http://orcid.org/0000-0001-5147-1273
Semmelweis University · HUEötvös Loránd University · HU

Funding

National Research, Development and Innovation Office NVKP_16-1-2016-0004New National Excellence Program of The Ministry of Human Capacities ÚNKP-17-4-III-SE-51New National Excellence Program of The Ministry of Human Capacities ÚNKP-17-4-I-SE-56
6 · The paper itself

Abstract

Up-regulation of the long non-coding RNA LINC00152 can contribute to cancer development, proliferation and invasion, including colorectal cancer, however, its mechanism of action in colorectal carcinogenesis and progression is only insufficiently understood. In this work we correlated LINC00152 expression with promoter DNA methylation changes in colorectal tissues along the normal-adenoma-carcinoma sequence and studied the effects of LINC00152 silencing on the cell cycle regulation and on the whole transcriptome in colon carcinoma cells using cell and molecular biology techniques. LINC00152 was significantly up-regulated in adenoma and colorectal cancer (p < 0.001) compared to normal samples, which was confirmed by real-time PCR and in situ hybridization. LINC00152 promoter hypomethylation detected in colorectal cancer (p < 0.01) was strongly correlated with increased LINC00152 expression (r=-0.90). Silencing of LINC00152 significantly suppressed cell growth, induced apoptosis and decreased cyclin D1 expression (p < 0.05). Whole transcriptome analysis of LINC00152-silenced cells revealed significant down-regulation of oncogenic and metastasis promoting genes (e.g. YES proto-oncogene 1, PORCN porcupine O-acyltransferase), and up-regulation of tumour suppressor genes (e.g. DKK1 dickkopf WNT signalling pathway inhibitor 1, PERP p53 apoptosis effector) (adjusted p < 0.05). Pathway analysis confirmed the LINC00152-related activation of oncogenic molecular pathways including those driven by PI3K/Akt, Ras, WNT, TP53, Notch and ErbB. Our results suggest that promoter hypomethylation related overexpression of LINC00152 can contribute to the pathogenesis of colorectal cancer by facilitating cell progression through the up-regulation of several oncogenic and metastasis promoting pathway elements.

Indexed as

DNA MethylationPromoter Regions, GeneticAgedBiomarkers, TumorCarcinogenesisCase-Control StudiesColorectal NeoplasmsFemaleFollow-Up StudiesGene Expression Regulation, NeoplasticHumansMaleMiddle AgedPrognosisProto-Oncogene MasRNA, Long NoncodingBiomarkers, Tumorlong non-coding RNA Linc00152, humanMAS1 protein, humanProto-Oncogene MasRNA, Long NoncodingColorectal adenomaColorectal cancerCYTORLINC00152Long non-coding RNA

Identifiers

PMID32307642
PMCPMC7471146
OpenAlexW3016519705

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.