Evidence map›Paper›PMID 37372319›Full record

ReviewGenes2023

JAK/STAT Signaling and Cervical Cancer: From the Cell Surface to the Nucleus.

Arturo Valle-Mendiola, Adriana Gutiérrez-Hoya, Isabel Soto-Cruz

Open access · goldAbstract readReview
In one paragraph

Review in Genes, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
12.0field-weighted citation impact, top 1% 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

42 citing papers in PubMed, 52 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Review
  6. ODF3B Promotes the Progression of Clear Cell Renal Cell Carcinoma via the JAK/STAT Signaling Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2026
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. STAT3 SH2 Domain Aspartic Acid 661 Mutations Activate Immune Gene Programs.Journal of cellular and molecular medicine · 2026
    Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Attributes of HPV associated cancers.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Review
  18. Article
  19. Article
  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

3 authors at 1 institution in 1 country.

Arturo Valle-MendiolaMolecular Oncology Laboratory, Cell Differentiation and Cancer Research Unit, FES Zaragoza, National University of Mexico, Batalla 5 de Mayo s/n, Colonia Ejército de Oriente, Mexico City 09230, Mexico.ORCID 0000-0001-6782-4547
Adriana Gutiérrez-HoyaMolecular Oncology Laboratory, Cell Differentiation and Cancer Research Unit, FES Zaragoza, National University of Mexico, Batalla 5 de Mayo s/n, Colonia Ejército de Oriente, Mexico City 09230, Mexico.
Isabel Soto-CruzMolecular Oncology Laboratory, Cell Differentiation and Cancer Research Unit, FES Zaragoza, National University of Mexico, Batalla 5 de Mayo s/n, Colonia Ejército de Oriente, Mexico City 09230, Mexico.ORCID 0000-0001-5115-3654
Secretaría de Ciencia, Humanidades, Tecnología e Innovación · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling pathway constitutes a rapid signaling module from the cell surface to the nucleus, and activates different cellular responses, such as proliferation, survival, migration, invasion, and inflammation. When the JAK/STAT pathway is altered, it contributes to cancer progression and metastasis. STAT proteins play a central role in developing cervical cancer, and inhibiting the JAK/STAT signaling may be necessary to induce tumor cell death. Several cancers show continuous activation of different STATs, including cervical cancer. The constitutive activation of STAT proteins is associated with a poor prognosis and overall survival. The human papillomavirus (HPV) oncoproteins E6 and E7 play an essential role in cervical cancer progression, and they activate the JAK/STAT pathway and other signals that induce proliferation, survival, and migration of cancer cells. Moreover, there is a crosstalk between the JAK/STAT signaling cascade with other signaling pathways, where a plethora of different proteins activate to induce gene transcription and cell responses that contribute to tumor growth. Therefore, inhibition of the JAK/STAT pathway shows promise as a new target in cancer treatment. In this review, we discuss the role of the JAK/STAT pathway components and the role of the HPV oncoproteins associated with cellular malignancy through the JAK/STAT proteins and other signaling pathways to induce tumor growth.

Indexed as

Papillomavirus InfectionsUterine Cervical NeoplasmsFemaleHumansJanus KinasesSignal TransductionSTAT Transcription FactorsJanus KinasesSTAT Transcription Factorscervical cancerHPVJAK/STAT pathwaysignaling

Identifiers

PMID37372319
PMCPMC10298571
OpenAlexW4378229735

What OpenQuestion 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 OpenQuestion graph.