Evidence map›Paper›PMID 37845209›Full record

ArticleCell death discovery2023

TRAF7-targeted HOXA5 acts as a tumor suppressor in prostate cancer progression and stemness via transcriptionally activating SPRY2 and regulating MEK/ERK signaling.

Jianfeng Ye, Wangmin Liu, Xueyang Yu, Lina Wu, Zhengjie Chen, Yufei Yu, Jianfeng Wang, Song Bai, Mo Zhang

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

9 citing papers in PubMed, 11 citations in OpenAlex.

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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

9 authors at 2 institutions in 1 country.

Jianfeng Ye *Department of Urology, Shengjing Hospital of China Medical University, Shenyang, Liaoning, China.
Wangmin Liu *Department of Urology, Shengjing Hospital of China Medical University, Shenyang, Liaoning, China.ORCID http://orcid.org/0000-0002-4060-5843
Xueyang Yu *Department of Urology, Shengjing Hospital of China Medical University, Shenyang, Liaoning, China.
Lina WuDepartment of Laboratory Medicine, Shengjing Hospital of China Medical University, Shenyang, Liaoning, China.
Zhengjie ChenDepartment of Urology, the First Hospital of China Medical University, Shenyang, Liaoning, China.
Yufei YuDepartment of Urology, the First Hospital of China Medical University, Shenyang, Liaoning, China.
Jianfeng WangDepartment of Urology, the First Hospital of China Medical University, Shenyang, Liaoning, China.
Song BaiDepartment of Urology, Shengjing Hospital of China Medical University, Shenyang, Liaoning, China. baisongcmu@163.com.
Mo ZhangDepartment of Urology, the First Hospital of China Medical University, Shenyang, Liaoning, China. peterzhang623@gmail.com.ORCID http://orcid.org/0000-0002-8405-8298
China Medical University · CNFirst Hospital of China Medical University · CN

Funding

Department of Education of Liaoning Province (Liaoning Provincial Education Department) No. LJKMZ20221138National Natural Science Foundation of China (National Science Foundation of China) No. 81802540National Natural Science Foundation of China (National Science Foundation of China) No. 82173372Natural Science Foundation of Liaoning Province (Liaoning Provincial Natural Science Foundation) No. 20180550985Shenyang Science and Technology Bureau (Science and Technology Bureau of Shenyang) No. RC190386
6 · The paper itself

Abstract

Homeobox A5 (HOXA5), a homeodomain transcription factor, is considered a tumor suppressor in cancer progression; however, its function in prostate cancer (PCa) remains unclear. This study focused on the relevance of HOXA5 in PCa progression. We identified the downregulation of HOXA5 in PCa tissues based on the TCGA database and further verified in 30-paired PCa and adjacent normal tissues. Functional studies revealed that HOXA5 upregulation impaired the stem-like characteristics and malignant behaviors of PCa cells in vitro and in vivo. Mechanistically, HOXA5 was found to be regulated by tumor necrosis factor receptor-associated factor 7 (TRAF7), a putative E3-ubiquitin ligase. We observed that TRAF7 was overexpressed in PCa and subsequently enhanced the degradation of HOXA5 protein via its ubiquitin ligase activity, contributing to the acquisition of an aggressive PCa phenotype. For its downstream mechanism, we demonstrated that sprouty RTK signaling antagonist 2 (SPRY2) served as a downstream target of HOXA5. HOXA5 could directly bind to the SPRY2 promoter, thereby regulating the SPRY2-mediated MEK/ERK signaling pathway. Silencing SPRY2 largely compromised the tumor-suppressive effect of HOXA5 in PCa progression and cancer stemness. Our findings highlight the previously-underappreciated signaling axis of TRAF7-HOXA5-SPRY2, which provides a novel prognostic and therapeutic target for PCa treatment.

Identifiers

PMID37845209
PMCPMC10579307
OpenAlexW4387665349

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.