Evidence map›Paper›PMID 42552468›Full record

ArticleActa pharmacologica Sinica2026

Secreted chimeric proteins as a strategy to correct SOX17 deficiency and attenuate the malignant phenotype of cholangiocarcinoma cells: a proof-of-concept study.

Ana Peleteiro-Vigil, Sara Ortiz-Rivero, Yanira Izquierdo-Mateo, Laura Sanchez-Vicente, Ester González-Sánchez, Javier Vaquero, Juan Carlos Arevalo, Oscar Briz, Maria J Monte, Jose J G Marin and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Acta pharmacologica Sinica, 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

11 authors.

Ana Peleteiro-Vigil *Experimental Hepatology and Drug Targeting (HEVEPHARM), Department of Physiology and Pharmacology, University of Salamanca, Salamanca, 37007, Spain.
Sara Ortiz-Rivero *Experimental Hepatology and Drug Targeting (HEVEPHARM), Department of Physiology and Pharmacology, University of Salamanca, Salamanca, 37007, Spain.
Yanira Izquierdo-MateoExperimental Hepatology and Drug Targeting (HEVEPHARM), Department of Physiology and Pharmacology, University of Salamanca, Salamanca, 37007, Spain.
Laura Sanchez-VicenteExperimental Hepatology and Drug Targeting (HEVEPHARM), Department of Physiology and Pharmacology, University of Salamanca, Salamanca, 37007, Spain.
Ester González-SánchezExperimental Hepatology and Drug Targeting (HEVEPHARM), Department of Physiology and Pharmacology, University of Salamanca, Salamanca, 37007, Spain.
Javier VaqueroExperimental Hepatology and Drug Targeting (HEVEPHARM), Department of Physiology and Pharmacology, University of Salamanca, Salamanca, 37007, Spain.
Juan Carlos ArevaloInstitute for Biomedical Research of Salamanca (IBSAL), Salamanca, 37007, Spain.
Oscar BrizExperimental Hepatology and Drug Targeting (HEVEPHARM), Department of Physiology and Pharmacology, University of Salamanca, Salamanca, 37007, Spain.
Maria J MonteExperimental Hepatology and Drug Targeting (HEVEPHARM), Department of Physiology and Pharmacology, University of Salamanca, Salamanca, 37007, Spain.
Jose J G MarinExperimental Hepatology and Drug Targeting (HEVEPHARM), Department of Physiology and Pharmacology, University of Salamanca, Salamanca, 37007, Spain. jjgmarin@usal.es.
Elisa HerraezExperimental Hepatology and Drug Targeting (HEVEPHARM), Department of Physiology and Pharmacology, University of Salamanca, Salamanca, 37007, Spain. elisah@usal.es.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cholangiocarcinoma (CCA) is a biliary cancer with a poor prognosis and marked chemoresistance. The transcription factor SOX17, which is essential for cholangiocyte differentiation, is frequently downregulated in CCA, as is the case with several tumor suppressor genes. This study provides a proof-of-concept for further development of cellular therapeutic strategies to restore SOX17 expression in CCA cells. For this aim, we used EGI-1 cells as the target cell model derived from extrahepatic CCA. Recombinant Tat-SOX17 protein was first produced in bacteria and purified using Ni-NTA affinity columns and asymmetric flow-field-flow fractionation. Tat-SOX17 entered EGI-1 cells and reached their nucleus. The addition of the α-fetoprotein signal peptide (AFPsp) to the chimeric protein enabled the efficient secretion of the fusion protein formed by AFPsp, SOX17, and reverse Tat (Tat

Indexed as

Cell-penetrating peptidesCell therapyDrug deliveryGene therapyLiver cancer

Identifiers

PMID42552468

What OpenQuestion 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 OpenQuestion graph.