Evidence map›Paper›PMID 35205666›Full record

ArticleCancers2022

SOX9 Triggers Different Epithelial to Mesenchymal Transition States to Promote Pancreatic Cancer Progression.

Estefania Carrasco-Garcia, Lidia Lopez, Veronica Moncho-Amor, Fernando Carazo, Paula Aldaz, Manuel Collado, Donald Bell, Ayman Gaafar, Eva Karamitopoulou, Alexandar Tzankov and 6 more

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.1field-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

15 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Article
  3. Role of SOX9 protein in ovarian carcinoma: A molecular insight.The Indian journal of medical research · 2026
    Review
  4. Article
  5. Review
  6. SOX9: an important factor in regulating breast cancer.European journal of medical research · 2025
    Review
  7. Article
  8. Deciphering of SOX9 Functions in Pancreatic Cancer Cells.International journal of molecular sciences · 2025
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
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

16 authors at 10 institutions in 4 countries.

Estefania Carrasco-GarciaCellular Oncology Group, Biodonostia Health Research Institute, 20014 San Sebastian, Spain.
Lidia LopezCellular Oncology Group, Biodonostia Health Research Institute, 20014 San Sebastian, Spain.
Veronica Moncho-AmorCellular Oncology Group, Biodonostia Health Research Institute, 20014 San Sebastian, Spain.ORCID 0000-0001-7914-6683
Fernando CarazoSchool of Engineering, University of Navarra, 20009 San Sebastian, Spain.ORCID 0000-0002-4288-3652
Paula AldazCellular Oncology Group, Biodonostia Health Research Institute, 20014 San Sebastian, Spain.
Manuel ColladoHealth Research Institute of Santiago de Compostela (IDIS), Xerencia de Xestión Integrada de Santiago (XXIS/SERGAS), 15706 Santiago de Compostela, Spain.ORCID 0000-0002-0330-0880
Donald BellThe Francis Crick Institute, London NW1 1AT, UK.ORCID 0000-0002-3788-1580
Ayman GaafarDepartment of Pathology, Cruces University Hospital, 48903 Barakaldo, Spain.ORCID 0000-0003-0324-2251
Eva KaramitopoulouInstitute of Pathology, University of Bern, 3012 Bern, Switzerland.
Alexandar TzankovInstitute of Pathology, University Hospital Basel, 4056 Basel, Switzerland.ORCID 0000-0002-1100-3819
Manuel HidalgoSpanish National Cancer Research Centre (CNIO), 28029 Madrid, Spain.
Ángel RubioSchool of Engineering, University of Navarra, 20009 San Sebastian, Spain.
Manuel SerranoInstitute for Research in Biomedicine (IRB Barcelona), Barcelona Institute of Science and Technology (BIST), 08028 Barcelona, Spain.ORCID 0000-0001-7177-9312
Charles H LawrieMolecular Oncology Group, Biodonostia Institute, 20014 San Sebastian, Spain.ORCID 0000-0002-8882-1131
Robin Lovell-BadgeThe Francis Crick Institute, London NW1 1AT, UK.ORCID 0000-0001-9364-4179
Ander MatheuCellular Oncology Group, Biodonostia Health Research Institute, 20014 San Sebastian, Spain.
Biogipuzkoa Health Research Institute · ESThe Francis Crick Institute · GBIkerbasque · ESUniversidad de Navarra · ESHospital de Cruces · ESInstitució Catalana de Recerca i Estudis Avançats · ESNewYork–Presbyterian Hospital · USServicio Gallego de Salud · ESUniversity Hospital of Basel · CHUniversity of Bern · CH

Funding

Instituto de Salud Carlos III PI16/01580
6 · The paper itself

Abstract

backgroundPancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers mainly due to spatial obstacles to complete resection, early metastasis and therapy resistance. The molecular events accompanying PDAC progression remain poorly understood. SOX9 is required for maintaining the pancreatic ductal identity and it is involved in the initiation of pancreatic cancer. In addition, SOX9 is a transcription factor linked to stem cell activity and is commonly overexpressed in solid cancers. It cooperates with Snail/Slug to induce epithelial-mesenchymal transition (EMT) during neural development and in diseases such as organ fibrosis or different types of cancer.

methodsWe investigated the roles of SOX9 in pancreatic tumor cell plasticity, metastatic dissemination and chemoresistance using pancreatic cancer cell lines as well as mouse embryo fibroblasts. In addition, we characterized the clinical relevance of SOX9 in pancreatic cancer using human biopsies.

resultsGain- and loss-of-function of SOX9 in PDAC cells revealed that high levels of SOX9 increased migration and invasion, and promoted EMT and metastatic dissemination, whilst SOX9 silencing resulted in metastasis inhibition, along with a phenotypic reversion to epithelial features and loss of stemness potential. In both contexts, EMT factors were not altered. Moreover, high levels of SOX9 promoted resistance to gemcitabine. In contrast, overexpression of SOX9 was sufficient to promote metastatic potential in

conclusionsOur results indicate that SOX9 facilitates PDAC progression and metastasis by triggering stemness and EMT.

Indexed as

chemoresistanceEMTmetastasispancreatic cancerplasticitySOX9

Identifiers

PMID35205666
PMCPMC8870732
OpenAlexW4213184384

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.