Evidence map›Paper›PMID 25595894›Full record

ArticleOncotarget2015

PATZ1 acts as a tumor suppressor in thyroid cancer via targeting p53-dependent genes involved in EMT and cell migration.

Gennaro Chiappetta, Teresa Valentino, Michela Vitiello, Rosa Pasquinelli, Mario Monaco, Giuseppe Palma, Romina Sepe, Antonio Luciano, Pierlorenzo Pallante, Dario Palmieri and 6 more

Open access · diamondAbstract readComparative Study
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

40 citing papers in PubMed, 52 citations in OpenAlex.

  1. Dysregulation of the PATZ1/CTCF Balance Silences ZBTB20 to Drive Melanoma Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  15. Structural analysis of the PATZ1 BTB domain homodimer.Acta crystallographica. Section D, Structural biology · 2020
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  16. Review
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  18. Clinical, pathological, and genomic features of EWSR1-PATZ1 fusion sarcoma.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2019
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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

16 authors at 4 institutions in 2 countries.

Gennaro ChiappettaDepartment of Experimental Oncology, Functional Genomic Unit, National Cancer Institute "Fondazione Giovanni Pascale", IRCCS, 80131 Naples, Italy.
Teresa ValentinoInstitute of Experimental Endocrinology and Oncology (IEOS), National Research Counsil (CNR), 80131 Naples, Italy.
Michela VitielloInstitute of Experimental Endocrinology and Oncology (IEOS), National Research Counsil (CNR), 80131 Naples, Italy.
Rosa PasquinelliDepartment of Experimental Oncology, Functional Genomic Unit, National Cancer Institute "Fondazione Giovanni Pascale", IRCCS, 80131 Naples, Italy.
Mario MonacoDepartment of Experimental Oncology, Functional Genomic Unit, National Cancer Institute "Fondazione Giovanni Pascale", IRCCS, 80131 Naples, Italy.
Giuseppe PalmaAnimal Facility, National Cancer Institute "Fondazione Giovanni Pascale", IRCCS, 80131 Naples, Italy.
Romina SepeInstitute of Experimental Endocrinology and Oncology (IEOS), National Research Counsil (CNR), 80131 Naples, Italy.
Antonio LucianoAnimal Facility, National Cancer Institute "Fondazione Giovanni Pascale", IRCCS, 80131 Naples, Italy.
Pierlorenzo PallanteInstitute of Experimental Endocrinology and Oncology (IEOS), National Research Counsil (CNR), 80131 Naples, Italy.
Dario PalmieriDepartments of Molecular Virology, Immunology and Human Genetics, Comprehensive Cancer Center, Ohio State University, Columbus, OH 43210, USA.
Concetta AielloDepartment of Experimental Oncology, Functional Genomic Unit, National Cancer Institute "Fondazione Giovanni Pascale", IRCCS, 80131 Naples, Italy.
Domenica ReaAnimal Facility, National Cancer Institute "Fondazione Giovanni Pascale", IRCCS, 80131 Naples, Italy.
Simona Nunzia LositoDepartment of Experimental Oncology, Functional Genomic Unit, National Cancer Institute "Fondazione Giovanni Pascale", IRCCS, 80131 Naples, Italy.
Claudio ArraAnimal Facility, National Cancer Institute "Fondazione Giovanni Pascale", IRCCS, 80131 Naples, Italy.
Alfredo FuscoInstitute of Experimental Endocrinology and Oncology (IEOS), National Research Counsil (CNR), 80131 Naples, Italy.
Monica FedeleInstitute of Experimental Endocrinology and Oncology (IEOS), National Research Counsil (CNR), 80131 Naples, Italy.
Istituto Nazionale Tumori IRCCS "Fondazione G. Pascale" · ITInstitute for Experimental Endocrinology and Oncology · ITThe Ohio State University · USUniversity of Naples Federico II · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

PATZ1, a POZ-Zinc finger protein, is emerging as an important regulator of development and cancer, but its cancer-related function as oncogene or tumor-suppressor is still debated. Here, we investigated its possible role in thyroid carcinogenesis. We demonstrated PATZ1 is down-regulated in thyroid carcinomas compared to normal thyroid tissues, with an inverse correlation to the degree of cell differentiation. In fact, PATZ1 expression was significantly further down-regulated in poorly differentiated and anaplastic thyroid cancers compared to the papillary histotype, and it resulted increasingly delocalized from the nucleus to the cytoplasm proceeding from differentiated to undifferentiated thyroid carcinomas. Restoration of PATZ1 expression in three thyroid cancer-derived cell lines, all characterized by fully dedifferentiated cells, significantly inhibited their malignant behaviors, including in vitro proliferation, anchorage-independent growth, migration and invasion, as well as in vivo tumor growth. Consistent with recent studies showing a role for PATZ1 in the p53 pathway, we showed that ectopic expression of PATZ1 in thyroid cancer cells activates p53-dependent pathways opposing epithelial-mesenchymal transition and cell migration to prevent invasiveness. These results provide insights into a potential tumor-suppressor role of PATZ1 in thyroid cancer progression, and thus may have potential clinical relevance for the prognosis and therapy of thyroid cancer.

Indexed as

Cell MovementEpithelial-Mesenchymal TransitionAnimalsApoptosisBlotting, WesternCarcinoma, PapillaryCell ProliferationChromatin ImmunoprecipitationFemaleGenes, Tumor SuppressorHumansImmunoenzyme TechniquesKruppel-Like Transcription FactorsMiceMice, NudeReal-Time Polymerase Chain ReactionKruppel-Like Transcription FactorsPATZ1 protein, humanRepressor ProteinsRNA, MessengerSERPINA3 protein, humanSerpinsTP53 protein, humanTumor Suppressor Protein p53cell migrationepithelial-mesenchymal transitionPATZ1thyroid cancer

Identifiers

PMID25595894
PMCPMC4467151
OpenAlexW2126511115

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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.