Evidence map›Paper›PMID 40869147›Full record

ReviewInternational journal of molecular sciences2025

The Role of Receptor Tyrosine Kinase-like Orphan Receptor 1 (ROR1) in Cancer Stem Cell Signaling.

Matthew S Jung, Won-Young Choi, Wenjing Zhang, Francisco N Barrera, Rachel S Perkins

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. Insulin-like growth factor receptor signaling in physiology and disease.Signal transduction and targeted therapy · 2026
    Review
  3. Imaging of ROR1 expression in tumors using radiolabeled affibody molecules.European journal of nuclear medicine and molecular imaging · 2026
    Article
  4. Translational cancer research · 2026
    Article
  5. 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

5 authors.

Matthew S JungDepartment of Pathology, College of Medicine, University of Tennessee Health Science Center, Memphis, TN 38163, USA.ORCID 0009-0005-1700-4870
Won-Young ChoiDepartment of Pathology, College of Medicine, University of Tennessee Health Science Center, Memphis, TN 38163, USA.ORCID 0009-0003-8276-2235
Wenjing ZhangDepartment of Pathology, College of Medicine, University of Tennessee Health Science Center, Memphis, TN 38163, USA.ORCID 0000-0002-6694-6072
Francisco N BarreraDepartment of Biochemistry and Cellular and Molecular Biology, College of Arts and Sciences, University of Tennessee, Knoxville, TN 37916, USA.
Rachel S PerkinsDepartment of Pathology, College of Medicine, University of Tennessee Health Science Center, Memphis, TN 38163, USA.ORCID 0000-0001-8780-3305

Funding

Mechanisms of modulation of transmembrane interactionsR35GM140846 · NIGMS · UNIVERSITY OF TENNESSEE KNOXVILLE · PI BARRERA, FRANCISCO NICOLAS · 2021 to 2025
$1.9M
NIGMS NIH HHS R35 GM140846NIH HHS 5R35GM140846-05University of Tennessee Oak Ridge Innovation Institute Development and Advancement of Radiopharmaceutical Therapies Convergent Research Initiative
6 · The paper itself

Abstract

Receptor tyrosine kinase-like orphan receptor 1 (ROR1) is a key regulator of cancer stem cell (CSC) biology and signaling. In CSCs, ROR1 acts as a receptor or co-receptor, interacting with non-canonical WNT ligands, and forming complexes with proteins like CD19 and HER2, to activate diverse downstream signaling pathways. ROR1 signaling in CSCs promotes proliferation, maintains stemness, and enhances migration, invasion, and the epithelial-to-mesenchymal transition (EMT). While minimally expressed after embryogenesis, ROR1 is aberrantly upregulated in numerous cancers, including ovarian, breast, pancreatic, and hematologic malignancies. ROR1 overexpression drives tumor progression, resistance to chemotherapies, disease recurrence, and ultimately metastasis. This expression pattern positions ROR1 as a promising target for CSC-specific therapies. High ROR1 expression is consistently linked to aggressive disease and poor patient outcomes. Here, we review ROR1's role in CSCs and highlight the complex signaling that is observed in the CSC population. Further, we evaluate the gaps in the current understanding of ROR1 signaling in CSCs and describe how ROR1 regulates the associated signaling pathways. Finally, we provide an up-to-date summary of the promising therapeutic strategies targeting ROR1 that overcome conventional cancer treatment limitations. This review highlights the role of ROR1 as a critical, functional driver of CSCs and adverse patient outcomes across various malignancies.

Indexed as

NeoplasmsNeoplastic Stem CellsReceptor Tyrosine Kinase-like Orphan ReceptorsSignal TransductionAnimalsEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansReceptor Tyrosine Kinase-like Orphan ReceptorsROR1 protein, humancancer stem cellsdrug resistancemetastasisROR1targeted therapy

Identifiers

PMID40869147
PMCPMC12386924

What Socratic holds

Textmetadata
LicenceCC BY
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.