Evidence map›Paper›PMID 40053212›Full record

SynthesisMolecular biology reports2025

Dead-End protein expression, function, and mutation in cancer: a systematic review.

Homa Faraji, Farnaz Banakar, Arash Sadri, Azadeh Ebrahim-Habibi

Abstract readSystematic Review
PubMed Publisher
In one paragraph

Synthesis in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Homa Faraji *Endocrinology and Metabolism Research Center, Endocrinology and Metabolism Clinical Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran.
Farnaz Banakar *Biosensor Research Center, Endocrinology and Metabolism Molecular-Cellular Sciences Institute, Tehran University of Medical Sciences, 10 Jalal-Al-Ahmad Street, Tehran, 1411713137, Iran. farnazban@gmail.com.
Arash SadriBiosensor Research Center, Endocrinology and Metabolism Molecular-Cellular Sciences Institute, Tehran University of Medical Sciences, 10 Jalal-Al-Ahmad Street, Tehran, 1411713137, Iran.
Azadeh Ebrahim-HabibiBiosensor Research Center, Endocrinology and Metabolism Molecular-Cellular Sciences Institute, Tehran University of Medical Sciences, 10 Jalal-Al-Ahmad Street, Tehran, 1411713137, Iran. aehabibi@sina.tums.ac.ir.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer incidence is rising globally, particularly in aging populations. Understanding the genetic, cellular, and molecular mechanisms underlying cancer is crucial for developing effective interventions. Dead-end protein 1 (DND1), an RNA-binding protein, plays a pivotal role in germ cell regulation and tumorigenesis. This systematic review investigates DND1's multifaceted roles in cancer progression and evaluates its interactions and potential as a therapeutic target. A systematic search of four databases (Web of Science, MEDLINE via PubMed, Scopus, and Embase) yielded 436 unique records. After screening, 38 studies were included for data extraction. STRING-based network analysis identified key interactors-including NANOS1-3, TDRD7, DAZL, and EIF2S2- and pathways associated with RNA binding, translational regulation, and apoptosis. DND1 demonstrates dual, context-dependent roles as both a tumor suppressor and promoter. Its regulation of miRNAs and interaction with germ cell-specific proteins emerged as critical mechanisms in tumor suppression and progression. This study highlights DND1's central role in cancer biology, with significant implications for diagnostics and therapeutics. The findings provide a robust foundation for experimental validation of key interactions and further exploration of DND1's molecular mechanisms. The dual functionality of DND1 as a tumor suppressor and promoter underscores its potential as a target for novel cancer therapies, particularly for germ cell tumors and other cancers.

Indexed as

NeoplasmsRNA-Binding ProteinsApoptosisCarcinogenesisGene Expression Regulation, NeoplasticHumansMicroRNAsMutationMicroRNAsRNA-Binding ProteinsGerm cellsmiRNANetwork analysisRNA binding proteinRRMTumorigenesis

Identifiers

What OpenQuestion holds

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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.