Evidence map›Paper›PMID 39014173›Full record

ArticleJournal of endocrinological investigation2024

PRDM1 promotes the ferroptosis and immune escape of thyroid cancer by regulating USP15-mediated SELENBP1 deubiquitination.

J Ma, Z Li, J Xu, J Lai, J Zhao, L Ma, X Sun

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Article in Journal of endocrinological investigation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

14 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Mechanistic insights into ferroptosis in thyroid cancer and its therapeutic implications.Apoptosis : an international journal on programmed cell death · 2026
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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

7 authors.

J MaDepartment of Vascular Surgery, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an City, 710004, Shaanxi, China.
Z LiDepartment of Vascular Surgery, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an City, 710004, Shaanxi, China.
J XuDepartment of General Surgery, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an City, 710004, Shaanxi, China.
J LaiDepartment of Vascular Surgery, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an City, 710004, Shaanxi, China.
J ZhaoDepartment of General Surgery, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an City, 710004, Shaanxi, China.
L MaDepartment of Laboratory Medicine, the First Affiliated Hospital of Xi'an Jiaotong University, Xi'an City, 710061, Shaanxi, China.
X SunDepartment of General Surgery, the First Affiliated Hospital of Xi'an Jiaotong University, No. 277 West Yanta Road, Xi'an City, 710061, Shaanxi, China. sunxy@mail.xjtu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe deubiquitinating enzyme Ubiquitin-specific peptidase 15 (USP15) is upregulated in various cancers and promotes tumor progression by increasing the expression of several oncogenes. This project is designed to explore the role and mechanism of USP15 in thyroid cancer (TC) progression.

methodsSelenium-binding protein 1 (SELENBP1), USP15, CCL2/5, CXCL10/11, IL-4, and TGF-β1 mRNA levels were detected using real-time quantitative polymerase chain reaction (RT-qPCR). SELENBP1, USP15, GPX4, IL-10, Arg-1, Granzyme B, TNF-α, and PR domain zinc finger protein 1 (PRDM1) protein levels were examined by western blot assay. Fe

resultsSELENBP1 was increased in TC subjects and cell lines, and its knockdown repressed TC cell proliferation, migration, invasion, immune escape, and induced ferroptosis in vitro, as well as blocked tumor growth in vivo. In mechanism, USP15 interacted with SELENBP1 and maintained its stabilization by removing ubiquitin. Meanwhile, the upregulation of USP15 was induced by the transcription factor PRDM1.

conclusionUSP15 transcriptionally mediated by PRDM1 might boost TC cell malignant behaviors through deubiquitinating SELENBP1, providing a promising therapeutic target for TC treatment.

Indexed as

FerroptosisPositive Regulatory Domain I-Binding Factor 1Selenium-Binding ProteinsThyroid NeoplasmsUbiquitin-Specific ProteasesAnimalsCell Line, TumorCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMice, NudeMiddle AgedTumor EscapePositive Regulatory Domain I-Binding Factor 1PRDM1 protein, humanSELENBP1 protein, humanSelenium-Binding ProteinsUbiquitin-Specific ProteasesUSP15 protein, humanFerroptosisImmune escapePRDM1SELENBP1Thyroid cancerUSP15

Identifiers

PMID39014173

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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.