Evidence map›Paper›PMID 31115798›Full record

ReviewMolecular diagnosis & therapy2019

S1PR1 as a Novel Promising Therapeutic Target in Cancer Therapy.

Narges Rostami, Afshin Nikkhoo, Amir Ajjoolabady, Gholamreza Azizi, Mohammad Hojjat-Farsangi, Ghasem Ghalamfarsa, Bahman Yousefi, Mehdi Yousefi, Farhad Jadidi-Niaragh

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular diagnosis & therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
2.3field-weighted citation impact, top 11% of its field
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

45 citing papers in PubMed, 72 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Sphingolipid Metabolism in the Pathogenesis of Hashimoto's Thyroiditis.International journal of molecular sciences · 2025
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Regulation of CXCR4 function by S1PCell communication and signaling : CCS · 2025
    Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Targeting Sphingosine-1-Phosphate Signaling in Breast Cancer.International journal of molecular sciences · 2024
    Review
  20. 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

9 authors at 4 institutions in 2 countries.

Narges RostamiDrug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Afshin NikkhooDrug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Amir AjjoolabadyResearch Center for Pharmaceutical Nanotechnology, Biomedicine Institute, Tabriz University of Medical Sciences, Tabriz, Iran.
Gholamreza AziziNon-Communicable Diseases Research Center, Alborz University of Medical Sciences, Karaj, Iran.
Mohammad Hojjat-FarsangiBioclinicum, Department of Oncology-Pathology, Karolinska Institute, Stockholm, Sweden.
Ghasem GhalamfarsaCellular and Molecular Research Center, Yasuj University of Medical Sciences, Yasuj, Iran.
Bahman YousefiDrug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Mehdi YousefiDrug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Farhad Jadidi-NiaraghImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. jadidif@tbzmed.ac.ir.ORCID 0000-0002-4641-882X
Tabriz University of Medical Sciences · IRJahrom University of Medical Sciences · IRKarolinska Institutet · SEYasuj University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sphingosine-1-phosphate (S1P) can regulate several physiological and pathological processes. S1P signaling via its cell surface receptor S1PR1 has been shown to enhance tumorigenesis and stimulate growth, expansion, angiogenesis, metastasis, and survival of cancer cells. S1PR1-mediated tumorigenesis is supported and amplified by activation of downstream effectors including STAT3, interleukin-6, and NF-κB networks. S1PR1 signaling can also trigger various other signaling pathways involved in carcinogenesis including activation of PI3K/AKT, MAPK/ERK1/2, Rac, and PKC/Ca, as well as suppression of cyclic adenosine monophosphate (cAMP). It also induces immunological tolerance in the tumor microenvironment, while the immunosuppressive function of S1PR1 can also lead to the generation of pre-metastatic niches. Some tumor cells upregulate S1PR1 signaling pathways, which leads to drug resistant cancer cells, mainly through activation of STAT3. This signaling pathway is also implicated in some inflammatory conditions leading to the instigation of inflammation-driven cancers. Furthermore, it can also increase survival via induction of anti-apoptotic pathways, for instance, in breast cancer cells. Therefore, S1PR1 and its signaling pathways can be considered as potential anti-tumor therapeutic targets, alone or in combination therapies. Given the oncogenic nature of S1PR1 and its distribution in a variety of cancer cell types along with its targeting advantages over other molecules of this family, S1PR1 should be considered a favorable target in therapeutic approaches to cancer. This review describes the role of S1PR1 in cancer development and progression, specifically addressing breast cancer, glioma, and hematopoietic malignancies. We also discuss the potential use of S1P signaling modulators as therapeutic targets in cancer therapy.

Indexed as

AnimalsAntineoplastic AgentsBiomarkers, TumorDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHumansInflammationMolecular Targeted TherapyNeoplasmsOrgan SpecificitySignal TransductionSphingosine-1-Phosphate ReceptorsStructure-Activity RelationshipTreatment OutcomeTumor MicroenvironmentAntineoplastic AgentsBiomarkers, TumorS1PR1 protein, humanSphingosine-1-Phosphate Receptors

Identifiers

PMID31115798
OpenAlexW2945503142

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.