Evidence map›Paper›PMID 42573585›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

Genetic Ablation and Multi-Omics Profiling Reveal CEP55 as a Key Driver of Tumorigenesis in Diverse Cancer Models.

Behnam Rashidieh, Yuanhao Yang, Amanda Louise Bain, Phillip Theron, Catharina Vosloo, Sahar Keshvari, Parinaz Ahangar, Brydie Bowden, Simon M Tria, Ben B Wang and 13 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. 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

23 authors.

Behnam RashidiehMater Research Institute, The University of Queensland, Translational Research Institute, Brisbane, QLD, Australia.ORCID https://orcid.org/0000-0002-9831-0319
Yuanhao YangMater Research Institute, The University of Queensland, Translational Research Institute, Brisbane, QLD, Australia.ORCID https://orcid.org/0000-0002-5857-0124
Amanda Louise BainCancer Research Program, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.
Phillip TheronMater Research Institute, The University of Queensland, Translational Research Institute, Brisbane, QLD, Australia.ORCID https://orcid.org/0009-0005-2518-1340
Catharina VoslooMater Research Institute, The University of Queensland, Translational Research Institute, Brisbane, QLD, Australia.
Sahar KeshvariMater Research Institute, The University of Queensland, Translational Research Institute, Brisbane, QLD, Australia.
Parinaz AhangarAustralian Institute for Bioengineering and Nanotechnology, The University of Queensland, Brisbane, Queensland, Australia.ORCID https://orcid.org/0000-0002-0060-3501
Brydie BowdenSchool of Environment and Science, Griffith University, Brisbane, QLD, Australia.
Simon M TriaCancer Research Program, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.
Ben B WangDepartment of Molecular & Cellular Biology, University of Adelaide, School of Biological Sciences, Adelaide, SA, Australia.
Sandra IsenmannSouth Australian Health and Medical Research Institute, Adelaide, SA, Australia.
Nicholas J Westra van HoltheAustralian Institute for Bioengineering and Nanotechnology, The University of Queensland, Brisbane, Queensland, Australia.ORCID https://orcid.org/0000-0002-0076-2967
Zherui XiongCancer Research Program, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.
Hani VuCancer Research Program, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.
Sowmya SharmaCancer Research Program, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.
Asmerom SengalMater Research Institute, The University of Queensland, Translational Research Institute, Brisbane, QLD, Australia.
J Alejandro LopezCancer Research Program, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.ORCID https://orcid.org/0000-0001-9370-1516
John FinnieSchool of Biomedicine, Faculty of Health and Medical Sciences, University of Adelaide, Adelaide, SA, Australia.ORCID https://orcid.org/0000-0003-2277-1693
Antonella PapaSouth Australian immunogenomics Cancer Institute, The University of Adelaide, Adelaide, South Australia, Australia.ORCID https://orcid.org/0000-0001-8653-7121
Pascal H G DuijfCentre for Cancer Biology, Clinical and Health Sciences, University of South Australia & SA Pathology, Adelaide, SA, Australia.
Quan NguyenCancer Research Program, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.ORCID https://orcid.org/0000-0001-7870-5703
Pirjo M ApajaDepartment of Molecular & Cellular Biology, University of Adelaide, School of Biological Sciences, Adelaide, SA, Australia.ORCID https://orcid.org/0000-0002-1622-2332
Kum Kum KhannaMater Research Institute, The University of Queensland, Translational Research Institute, Brisbane, QLD, Australia.

Funding

National Breast Cancer Foundation (NBCF) Investigator Initiated Research Scheme 2023/IIRS0077National Health & Medical Research Council (NH&MRC) Program ID 1017028Victorian Cancer Agency Mid-Career Research Fellowships MCRF20027
6 · The paper itself

Abstract

CEP55, a centrosomal protein frequently overexpressed in multiple cancers, is implicated in regulation of genomic instability and PI3K/AKT pathway activation, yet its role in tumor progression and the tumor microenvironment remains incompletely defined. Here, we developed an inducible Cep55 knockout (KO) mouse model and complementary primary, immortalized, and transformed mouse embryonic fibroblast (MEF) systems and employ integrative multi-omics analyses to define CEP55-driven mechanisms and validated findings in human cancer datasets. Cep55 deletion is well tolerated in adult tissues but significantly delays tumor onset and progression in E1A/Ras-driven models and prolongs survival in PTEN-deficient cancer models. Mechanistically, spatial transcriptomic and proteomic analyses revealed that CEP55 regulates extracellular matrix (ECM) remodeling, integrin signaling, and cell adhesion pathways, AKT/ERK signaling and cellular stress responses. Importantly, loss of Cep55 also reprograms the tumor immune microenvironment, reducing tumor-supportive macrophage polarization and enhancing antigen-specific CD8

Indexed as

CEP55integrin and PI3K/AKT pathwaysPTENtumorigenesis

Identifiers

PMID42573585
PMCPMC13455837

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.