Evidence mapPaperPMID 41226317Full record

SynthesisInternational journal of molecular sciences2025

ERO1α as a Potential Drug Target for Breast Cancer: A Systematic Review of Current Evidence.

Kamilla Khojayeva, Aiman Moldasheva, Mohamad Aljofan

Abstract readSystematic Review
In one paragraph

Synthesis in International journal of molecular sciences, 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

3 authors.

Kamilla KhojayevaDepartment of Biomedical Sciences, School of Medicine Nazarbayev University, Astana 010000, Kazakhstan.ORCID 0009-0009-2019-4491
Aiman MoldashevaDepartment of Biomedical Sciences, School of Medicine Nazarbayev University, Astana 010000, Kazakhstan.
Mohamad AljofanDepartment of Biomedical Sciences, School of Medicine Nazarbayev University, Astana 010000, Kazakhstan.

Funding

Nazarbayev University OPCRP2025017
6 · The paper itself

Abstract

Hypoxia, oxidative stress, and impaired protein folding contribute to tumor progression and therapy resistance. Endoplasmic Reticulum Oxidoreductin 1 Alpha (ERO1α) is a key enzyme regulating redox homeostasis in the endoplasmic reticulum by reoxidizing protein disulfide isomerase, facilitating disulfide bond formation, and generating reactive oxygen species. Elevated ERO1α levels are associated with increased tumor aggressiveness, metastasis, and poor clinical outcomes. Despite growing evidence of its tumor-promoting functions, no clinically approved ERO1α inhibitors exist. This systematic review provides a comprehensive and integrative analysis of current research on ERO1α in breast cancer, emphasizing its roles in hypoxia response, angiogenesis, immune modulation, and ferroptosis resistance. We discuss mechanistic links, including VEGF-A maturation and PD-L1-mediated immune evasion, and highlight recent advances in small-molecule ERO1α inhibitors and preclinical therapeutic strategies. By consolidating molecular insights and translational considerations, this review underscores ERO1α as both a promising therapeutic target and potential prognostic marker, offering guidance for future drug development and targeted interventions in redox-dependent cancer pathways.

Indexed as

Antineoplastic AgentsBreast NeoplasmsMembrane GlycoproteinsOxidoreductasesAnimalsFemaleHumansMolecular Targeted TherapyAntineoplastic AgentsERO1A protein, humanMembrane GlycoproteinsOxidoreductasesbreast cancerdrug targetERO1αoxidative stress

Identifiers

PMID41226317
PMCPMC12608624

What Socratic holds

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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 Socratic graph.