Evidence map›Paper›PMID 26225839›Full record

ArticleCancer letters2015

Integrated genomic analyses identify KDM1A's role in cell proliferation via modulating E2F signaling activity and associate with poor clinical outcome in oral cancer.

Sathiya Pandi Narayanan, Smriti Singh, Amit Gupta, Sandhya Yadav, Shree Ram Singh, Sanjeev Shukla

Open access · greenAbstract read
In one paragraph

Article in Cancer letters, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 26% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
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  6. The HNRNPA2B1-MST1R-Akt axis contributes to epithelial-to-mesenchymal transition in head and neck cancer.Laboratory investigation; a journal of technical methods and pathology · 2020
    Article
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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

6 authors at 1 institution in 2 countries.

Sathiya Pandi NarayananEpigenetics and RNA Processing Laboratory (ERPL), Indian Institute of Science Education and Research Bhopal (IISERB), Madhya Pradesh, India.
Smriti SinghEpigenetics and RNA Processing Laboratory (ERPL), Indian Institute of Science Education and Research Bhopal (IISERB), Madhya Pradesh, India.
Amit GuptaEpigenetics and RNA Processing Laboratory (ERPL), Indian Institute of Science Education and Research Bhopal (IISERB), Madhya Pradesh, India.
Sandhya YadavEpigenetics and RNA Processing Laboratory (ERPL), Indian Institute of Science Education and Research Bhopal (IISERB), Madhya Pradesh, India.
Shree Ram SinghBasic Research Laboratory, Center for Cancer Research, National Cancer Institute, Frederick, MD 21702, USA. Electronic address: singhshr@mail.nih.gov.
Sanjeev ShuklaEpigenetics and RNA Processing Laboratory (ERPL), Indian Institute of Science Education and Research Bhopal (IISERB), Madhya Pradesh, India. Electronic address: sanjeevs@iiserb.ac.in.
Indian Institute of Science Education and Research, Bhopal · IN

Funding

Molecular Genetic Study of Stem Cells, Cancer Stem Cells, and Stem Cell AgingZIABC010738 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HOU, STEVEN · 2009 to 2020
$14.4M
Intramural NIH HHS Z99 CA999999Intramural NIH HHS ZIA BC010738
6 · The paper itself

Abstract

The histone demethylase KDM1A specifically demethylates lysine residues and its deregulation has been implicated in the initiation and progression of various cancers. However, KDM1A's molecular role and its pathological consequences, and prognostic significance in oral cancer remain less understood. In the present study, we sought to investigate the expression of KDM1A and its downstream role in oral cancer pathogenesis. By comparing mRNA expression profiles, we identified an elevated KDM1A expression in oral tumors when compared to normal oral tissues. In silico pathway prediction identified the association between KDM1A and E2F1 signaling in oral cancer. Pathway scanning, functional annotation analysis and In vitro assays showed the KDM1A's involvement in oral cancer cell proliferation and the cell cycle. Moreover, real time PCR and luciferase assays confirmed KDM1A's role in regulation of E2F1 signaling activity in oral cancer. Elevated KDM1A expression is associated with poor clinical outcome in oral cancer. Our data indicate that deregulated KDM1A expression is positively associated with proliferative phenotype of oral cancer and confers poor clinical outcome. These cumulative data suggest that KDM1A might be a potential diagnostic and therapeutic target for oral cancer.

Indexed as

Cell ProliferationBiomarkers, TumorCell Line, TumorComputer SimulationE2F1 Transcription FactorGene Expression ProfilingGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticGene Regulatory NetworksGenetic Association StudiesHistone DemethylasesHumansMouth NeoplasmsPhenotypePrognosisProportional Hazards ModelsBiomarkers, TumorE2F1 protein, humanE2F1 Transcription FactorHistone DemethylasesKDM1A protein, humanRNA, MessengerCell proliferationE2F1 signalingHistone demethylaseKDM1AOral cancer

Identifiers

PMID26225839
PMCPMC7751892
OpenAlexW1516176393

What OpenQuestion holds

Textmetadata
LicenceTDM
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.