Evidence map›Paper›PMID 41188771›Full record

SynthesisBMC cancer2025

Clinical and mechanistic insights into the expression of SP100 family proteins in various cancers: a systematic review.

Mehrnoosh Azami, Fatemeh Sadeghi, Nazanin Mohammadi, Zahra Sadat Shayegh, Arshia Hassanzadeh, Mohammad Javad Heidarzadeh, Armin ZarinKhat, Zhina Mohamadi

Abstract readSystematic Review
In one paragraph

Synthesis in BMC cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

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

  1. Pooled it
  2. Review
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

8 authors.

Mehrnoosh Azami *Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran.ORCID http://orcid.org/0009-0005-9044-8830
Fatemeh Sadeghi *Tehran branch, Faculty of Medicine, Islamic Azad University of Medical Sciences, Tehran, Iran.ORCID http://orcid.org/0000-0002-6762-4745
Nazanin Mohammadi *Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran.ORCID http://orcid.org/0009-0009-4166-494X
Zahra Sadat Shayegh *Islamic Azad University of Tehran- Medical Branch, Tehran, Iran.ORCID http://orcid.org/0009-0008-8726-926X
Arshia HassanzadehFaculty of Medicine, Iran University of Medical Sciences, Tehran, Iran.ORCID http://orcid.org/0009-0005-9433-7476
Mohammad Javad HeidarzadehFaculty of Medicine, Ahvaz University of Medical Sciences, Ahvaz, Khouzestan, Iran.
Armin ZarinKhat *Faculty of medicine, Kermanshah University of medical sciences, Shahid beheshti Blvd, Kermanshah, 6715847141, Iran. zkharmin@gmail.com.
Zhina Mohamadi *Faculty of medicine, Kermanshah University of medical sciences, Shahid beheshti Blvd, Kermanshah, 6715847141, Iran. zhinamohamadi22@gmail.com.ORCID http://orcid.org/0009-0007-6862-0379

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionCancer remains a leading global health burden, with projections estimating 35 million new cases by 2050. The Speckled Protein 100 (SP100) family, comprising SP100, SP110, SP140, and SP140L, has emerged as a critical player in cancer biology due to their roles in transcriptional regulation, chromatin modification, and immune signaling. While SP100 acts as a tumor suppressor in malignancies like breast cancer, SP110 and SP140 are implicated in promoting oral squamous cell carcinoma and glioma progression, respectively, and SP140L is linked to poor prognosis in pancreatic adenocarcinoma. Despite growing evidence of their dual oncogenic and tumor-suppressive functions across cancers, inconsistencies in expression patterns, regulatory mechanisms, and clinical implications persist. The current review of the SP100 family’s roles in cancer aims to clarify any direct future translational research to enhance cancer outcomes.

methodFollowing PRISMA guidance, a comprehensive search was conducted in several databases (PubMed, Scopus, Web of Science, and Google Scholar). After RAYYAN-assisted deduplication and screening, studies analyzing SP100, SP110, SP140, or SP140L alterations in human cancers (excluding cell lines studies) were included. Data on genetic/epigenetic changes, cancer types, and clinical outcomes were extracted, with quality assessed via standardized tools.

resultsThis systematic review analyzed 29 studies (2004–2024) to evaluate the dual roles of SP100 family proteins (SP100, SP110, SP140, SP140L) across 25 cancer types. SP100 exhibited context-dependent roles: high expression correlated with better prognosis in breast/lung cancers but poorer outcomes in glioma/PAAD, while low expression in LSCC was linked to tumorigenesis. SP110 overexpression was tied to poor prognosis in oral, lung, and renal cancers but was protective in DLBCL. SP140, the most studied member, showed divergent associations: high expression worsened outcomes in ccRCC, glioma, and gynecologic cancers but improved survival in AML, osteosarcoma, and melanoma. Genetic/epigenetic alterations (mutations, copy number loss, and methylation) influenced prognosis in hematologic and solid tumors. SP140L, the least explored, correlated with poor PAAD prognosis.

conclusionThis study highlights the dual oncogenic/tumor-suppressive roles of SP100 family proteins across cancers. It also introduces this family as a therapeutic target. Further, it underscores their prognostic value in hematologic and solid tumors, highlighting SP140 as a key biomarker and SP100/SP140 inhibitors as promising strategies. Geographic bias and limited SP140L data reveal gaps; Future research should include multi-center studies, standardized methods, and mechanistic exploration of SP140L and SP110 in the immune microenvironment. Prioritizing clinical trials targeting SP100 family members could advance precision oncology and immunotherapy integration.

Indexed as

NeoplasmsBiomarkers, TumorGene Expression Regulation, NeoplasticHumansPrognosisBiomarkers, TumorCancerNeoplasmSP100SP110SP140SP140L

Identifiers

PMID41188771
PMCPMC12584231

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.