Evidence map›Paper›PMID 42225648›Full record

ArticleCell death discovery2026

Disruption of thrombospondin 1/2-integrin β1 axis impairs cell adhesion and tumor growth in intrahepatic cholangiocarcinoma.

Veronica Porreca, Ludovica Giancola, Luca Sallustio, Alessia Conigliaro, Pietro Angelone, Roberta Marrone, Francesco Greco, Dionino Marco Giangrande, Giulio Bontempi, Michele Stella and 15 more

Abstract read
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In one paragraph

Article in Cell death discovery, 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

25 authors.

Veronica PorrecaDepartment of Molecular Medicine, Sapienza University of Rome, Viale del Policlinico 155, 00161, Rome, Italy.
Ludovica GiancolaDepartment of Molecular Medicine, Sapienza University of Rome, Viale del Policlinico 155, 00161, Rome, Italy.
Luca SallustioDepartment of Molecular Medicine, Sapienza University of Rome, Viale del Policlinico 155, 00161, Rome, Italy.
Alessia ConigliaroDepartment of Molecular Medicine, Sapienza University of Rome, Viale del Policlinico 155, 00161, Rome, Italy.
Pietro AngeloneDepartment of Molecular Medicine, Sapienza University of Rome, Viale del Policlinico 155, 00161, Rome, Italy.
Roberta MarroneDepartment of Molecular Medicine, Sapienza University of Rome, Viale del Policlinico 155, 00161, Rome, Italy.
Francesco GrecoDepartment of Molecular Medicine, Sapienza University of Rome, Viale del Policlinico 155, 00161, Rome, Italy.
Dionino Marco GiangrandeDepartment of Molecular Medicine, Sapienza University of Rome, Viale del Policlinico 155, 00161, Rome, Italy.
Giulio BontempiDepartment of Molecular Medicine, Sapienza University of Rome, Viale del Policlinico 155, 00161, Rome, Italy.
Michele StellaDepartment of Biomedical and Biotechnological Sciences, Section of Biology and Genetics "G. Sichel", University of Catania, 95123, Catania, Italy.
Biagio PalmisanoDepartment of Molecular Medicine, Sapienza University of Rome, Viale del Policlinico 155, 00161, Rome, Italy.
Giuseppina MignognaDepartment of Biochemistry Science, Sapienza University of Rome, P.le Aldo Moro 5, 00185, Rome, Italy.
Martina MeucciDepartment of Anatomy, Histology, Forensic Medicine and Orthopedics, Unit of Histology and Medical Embryology, Sapienza University, Rome, Italy.
Fabio MelandroGeneral Surgery and Organ Transplantation Unit, Department of General Surgery and Surgical Specialties P. Stefanini, Sapienza University of Rome, Rome, Italy.
Gianluca MenniniGeneral Surgery and Organ Transplantation Unit, Department of General Surgery and Surgical Specialties P. Stefanini, Sapienza University of Rome, Rome, Italy.
Massimo RossiGeneral Surgery and Organ Transplantation Unit, Department of General Surgery and Surgical Specialties P. Stefanini, Sapienza University of Rome, Rome, Italy.
Mara RiminucciDepartment of Molecular Medicine, Sapienza University of Rome, Viale del Policlinico 155, 00161, Rome, Italy.ORCID http://orcid.org/0000-0002-8643-9211
Alessandro CorsiDepartment of Molecular Medicine, Sapienza University of Rome, Viale del Policlinico 155, 00161, Rome, Italy.ORCID http://orcid.org/0000-0001-6896-4509
Helena StabileDepartment of Molecular Medicine, Sapienza University of Rome, Viale del Policlinico 155, 00161, Rome, Italy.
Marco RagusaDepartment of Biomedical and Biotechnological Sciences, Section of Biology and Genetics "G. Sichel", University of Catania, 95123, Catania, Italy.
Antonio FilippiniDepartment of Anatomy, Histology, Forensic Medicine and Orthopedics, Unit of Histology and Medical Embryology, Sapienza University, Rome, Italy.ORCID http://orcid.org/0000-0001-8453-287X
Valerio FulciDepartment of Molecular Medicine, Sapienza University of Rome, Viale del Policlinico 155, 00161, Rome, Italy.
Raffaele StrippoliDepartment of Molecular Medicine, Sapienza University of Rome, Viale del Policlinico 155, 00161, Rome, Italy.ORCID http://orcid.org/0000-0003-3483-8381
Bruno MarasDepartment of Biochemistry Science, Sapienza University of Rome, P.le Aldo Moro 5, 00185, Rome, Italy.
Carmine ManconeDepartment of Molecular Medicine, Sapienza University of Rome, Viale del Policlinico 155, 00161, Rome, Italy. carmine.mancone@uniroma1.it.ORCID http://orcid.org/0000-0002-9569-5030

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Elevated expression of THBS1 and THBS2 in intrahepatic cholangiocarcinoma (iCCA) contributes to tumor growth and metastatic dissemination. Both proteins are predominantly produced by cancer-associated fibroblasts (CAFs) and iCCA cells, enhancing the interaction of malignant cholangiocytes with the extracellular matrix (ECM). Here, we identify integrin α3β1 and α6β1 as the cognate receptors for THBS1 and THBS2 on iCCA cell surface. Disruption of the THBS1-integrin β1 axis via monoclonal antibodies, THBS1-derived peptides, or THBS1 knockout (KO) iCCA cells reduces autocrine and paracrine integrin β1 activation, resulting in decreased ECM adhesion in both two-dimensional and three-dimensional assays. Loss of endogenous THBS1 also alters cell morphology, weakens intracellular junctions, and prevents tumor formation in mouse xenograft models. These findings identify the THBS1/THBS2-integrin β1 axis as a key driver of iCCA cell adhesion and malignancy, supporting its potential as a therapeutic target for iCCA-specific interventions.

Identifiers

PMID42225648
PMCPMC13438543

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