Evidence map›Paper›PMID 39212334›Full record

ArticleCell proliferation2025

Splicing control by PHF5A is crucial for melanoma cell survival.

Tina Meißgeier, Melanie Kappelmann-Fenzl, Sebastian Staebler, Ata Jadid Ahari, Christian Mertes, Julien Gagneur, Lisa Linck-Paulus, Anja Katrin Bosserhoff

Abstract read
In one paragraph

Article in Cell proliferation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
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.

Tina MeißgeierInstitute of Biochemistry, Friedrich-Alexander-University Erlangen-Nürnberg (FAU), Erlangen, Germany.ORCID https://orcid.org/0009-0005-9309-8522
Melanie Kappelmann-FenzlInstitute of Biochemistry, Friedrich-Alexander-University Erlangen-Nürnberg (FAU), Erlangen, Germany.ORCID https://orcid.org/0000-0003-0312-1687
Sebastian StaeblerInstitute of Biochemistry, Friedrich-Alexander-University Erlangen-Nürnberg (FAU), Erlangen, Germany.ORCID https://orcid.org/0000-0002-3772-477X
Ata Jadid AhariSchool of Computation, Information and Technology, Technical University of Munich, Garching, Germany.ORCID https://orcid.org/0009-0004-1577-7733
Christian MertesSchool of Computation, Information and Technology, Technical University of Munich, Garching, Germany.ORCID https://orcid.org/0000-0002-1091-205X
Julien GagneurSchool of Computation, Information and Technology, Technical University of Munich, Garching, Germany.ORCID https://orcid.org/0000-0002-8924-8365
Lisa Linck-PaulusInstitute of Biochemistry, Friedrich-Alexander-University Erlangen-Nürnberg (FAU), Erlangen, Germany.ORCID https://orcid.org/0000-0001-8581-684X
Anja Katrin BosserhoffInstitute of Biochemistry, Friedrich-Alexander-University Erlangen-Nürnberg (FAU), Erlangen, Germany.ORCID https://orcid.org/0000-0001-8147-394X

Funding

Bayerisches Staatsministerium für Wissenschaft und KunstDeutsche Forschungsgemeinschaft BO1573NFDI 1/1 4419
6 · The paper itself

Abstract

Abnormalities in alternative splicing are a hallmark of cancer formation. In this study, we investigated the role of the splicing factor PHD finger protein 5A (PHF5A) in melanoma. Malignant melanoma is the deadliest form of skin cancer, and patients with a high PHF5A expression show poor overall survival. Our data revealed that an siRNA-mediated downregulation of PHF5A in different melanoma cell lines leads to massive splicing defects of different tumour-relevant genes. The loss of PHF5A results in an increased rate of apoptosis by triggering Fas- and unfolded protein response (UPR)-mediated apoptosis pathways in melanoma cells. These findings are tumour-specific because we did not observe this regulation in fibroblasts. Our study identifies a crucial role of PHF5A as driver for melanoma malignancy and the described underlying splicing network provides an interesting basis for the development of new therapeutic targets for this aggressive form of skin cancer.

Indexed as

Alternative SplicingMelanomaSkin NeoplasmsApoptosisCell Line, TumorCell SurvivalGene Expression Regulation, NeoplasticHumansRNA, Small InterferingRNA Splicing FactorsUnfolded Protein ResponseRNA, Small InterferingRNA Splicing Factors

Identifiers

PMID39212334
PMCPMC11839196

What Socratic holds

Textmetadata
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.