Evidence map›Paper›PMID 24983967›Full record

ArticlePloS one2014

Trim28 contributes to EMT via regulation of E-cadherin and N-cadherin in lung cancer cell lines.

Lu Chen, Teresita Muñoz-Antonia, W Douglas Cress

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

57 citing papers in PubMed, 82 citations in OpenAlex.

  1. Proteomic profiling of CD133 + and CD326 + (EpCAM) subpopulations in A549 cells: insights into pluripotency and tumor heterogeneity.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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  10. Non-small cell lung cancer map and analysis: exploring interconnected oncogenic signal integrators.Mammalian genome : official journal of the International Mammalian Genome Society · 2025
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  11. Multifaceted role ofMedComm · 2024
    Review
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  15. TRIM28 in cancer and cancer therapy.Frontiers in genetics · 2024
    Review
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  17. Review
  18. A TIAM1-TRIM28 complex mediates epigenetic silencing of protocadherins to promote migration of lung cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2023
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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

3 authors at 2 institutions in 1 country.

Lu ChenMolecular Oncology Program, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, United States of America.
Teresita Muñoz-AntoniaMolecular Oncology Program, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, United States of America.
W Douglas CressMolecular Oncology Program, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, United States of America.
Moffitt Cancer Center · USMolecular Oncology (United States) · US

Funding

TRANSLATIONAL RESEARCHP30CA076292 · NCI · UNIVERSITY OF SOUTH FLORIDA · PI KENNETH Lynn WRIGHT · 1998 to 2026
$93.5M
Using MC1R genotype to impact skin cancer risk behaviors in Hispanics/LatinosU54CA163068 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI KENNETH Lynn WRIGHT · 2012 to 2026
$23.1M
SPORE in Lung CancerP50CA119997 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI GABRILOVICH, DMITRY I · 2008 to 2012
$11.0M
NCI NIH HHS CA119997NCI NIH HHS CA163068NCI NIH HHS P30 CA076292NCI NIH HHS P50 CA119997NCI NIH HHS U54 CA163068
6 · The paper itself

Abstract

In previous work, we demonstrated that transcription factor Trim28 (Tripartite motif containing 28) plays a tumor-suppressor role in early-staged adenocarcinoma of the lung due to its ability to restrain transcription of cell cycle-regulating genes. Herein we examine Trim28's role in the epithelial-to-mesenchymal transition (EMT) which is strongly implicated in cancer metastasis. We found that Trim28 plays a role in TGF-β-induced EMT in non-small cell lung cancer cells. Silencing Trim28 with inhibitory RNAs alters the expression of numerous EMT markers, such as E-cadherin and N-cadherin, whereas overexpression of Trim28 has an opposite effect. Trim28 expression is induced following TGF-β treatment at both protein and mRNA levels. Trim28 deficiency impairs TGF-β-induced EMT and decreases cell migration and invasion. Finally, we demonstrate that the expression of Trim28 affects the acetylation and methylation of histones on E-cadherin and N-cadherin promoters. These results suggest that Trim28 contributes to EMT and might be important for tumor metastasis in lung cancer. Taken together with our previous work these results suggest a model in which Trim28 is a tumor suppressor early in the transformation process in lung cancer, but in later stages it functions as an oncogene.

Indexed as

Biomarkers, TumorCadherinsCell Line, TumorEpithelial-Mesenchymal TransitionHumansLung NeoplasmsRepressor ProteinsTransforming Growth Factor betaTripartite Motif-Containing Protein 28Biomarkers, TumorCadherinsRepressor ProteinsTransforming Growth Factor betaTRIM28 protein, humanTripartite Motif-Containing Protein 28

Identifiers

PMID24983967
PMCPMC4077753
OpenAlexW2086277239

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.