Evidence map›Paper›PMID 31142791›Full record

ArticleScientific reports2019

Mechanistic Study of TTF-1 Modulation of Cellular Sensitivity to Cisplatin.

Cody A Phelps, Laura Lindsey-Boltz, Aziz Sancar, David Mu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.3field-weighted citation impact, top 41% 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

6 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Significance ofPeerJ · 2024
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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

4 authors at 3 institutions in 1 country.

Cody A PhelpsLeroy T. Canoles Jr. Cancer Research Center, Eastern Virginia Medical School, Norfolk, VA, 23501, USA.
Laura Lindsey-BoltzDepartment of Biochemistry and Biophysics, University of North Carolina School of Medicine, Chapel Hill, NC, 27599, USA.ORCID http://orcid.org/0000-0001-6493-8194
Aziz SancarDepartment of Biochemistry and Biophysics, University of North Carolina School of Medicine, Chapel Hill, NC, 27599, USA.
David MuLeroy T. Canoles Jr. Cancer Research Center, Eastern Virginia Medical School, Norfolk, VA, 23501, USA. mud@evms.edu.ORCID http://orcid.org/0000-0002-7762-0182
University of North Carolina at Chapel Hill · USCarter Center · USEastern Virginia Medical School · US

Funding

UNC-CH CENTER FOR ENVIRONMENTAL HEALTH &SUSCEPTIBILITYP30ES010126 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Stephanie Engel · 2001 to 2026
$36.3M
Molecular Mechanism of Mammalian DNA Excision Repair, DNA Damage Checkpoints and the Circadian ClockR35GM118102 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI AZIZ SANCAR · 2016 to 2026
$10.6M
Single Nucleotide Resolution Map of Formation and Repair of Bulky Adducts in the Human GenomeR01ES027255 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SANCAR, AZIZ · 2016 to 2020
$2.3M
Modifier of Cancer Sensitivity to StatinsR21CA198327 · NCI · EASTERN VIRGINIA MEDICAL SCHOOL · PI MU, DAVID · 2016 to 2017
$351k
NCI NIH HHS R21 CA198327NIEHS NIH HHS P30 ES010126NIEHS NIH HHS R01 ES027255NIGMS NIH HHS R35 GM118102
6 · The paper itself

Abstract

The lung lineage master regulator gene, Thyroid Transcription Factor-1 (TTF-1, also known as NKX2-1), is used as a marker by pathologists to identify lung adenocarcinomas since TTF-1 is expressed in 60 ~ 70% of lung ADs. Much research has been conducted to investigate roles of TTF-1 in lung cancer biology. But, how it modulates cellular chemosensitivity remains poorly characterized. Our study shows that TTF-1 sensitizes the KRAS-mutated A549 and NCI-H460 lung cancer cells to cisplatin, a common chemotherapy used to treat lung cancer. This chemosensitization activity does not appear to be mediated by a TTF-1-imposed alteration on nucleotide excision repair. Mechanistically, TTF-1 induced a reduction in p-AKT (S473), which in turn activated glycogen synthase kinase 3 (GSK3) and reduced β-catenin. Intriguingly, in the EGFR-mutated NCI-H1975 and HCC827 cells, TTF-1 desensitized these cells to cisplatin; concomitantly, TTF-1 conferred an increase in p-AKT. Finally, the conditioned media of TTF-1-transefected cells sensitized TTF-1

Indexed as

A549 CellsAdenocarcinoma of Lungbeta CateninBiomarkers, TumorCell LineageCisplatinDrug Resistance, NeoplasmErbB ReceptorsGene Expression Regulation, NeoplasticGlycogen Synthase Kinase 3HumansProto-Oncogene Proteins c-aktProto-Oncogene Proteins p21(ras)Thyroid Nuclear Factor 1beta CateninBiomarkers, TumorCisplatinCTNNB1 protein, humanEGFR protein, humanErbB ReceptorsGlycogen Synthase Kinase 3KRAS protein, humanProto-Oncogene Proteins c-aktProto-Oncogene Proteins p21(ras)Thyroid Nuclear Factor 1

Identifiers

PMID31142791
PMCPMC6541604
OpenAlexW2947535484

What OpenQuestion holds

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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.