Evidence map›Paper›PMID 28388884›Full record

ArticleBMC cancer2017

Inhibition of Six1 affects tumour invasion and the expression of cancer stem cell markers in pancreatic cancer.

Tristan Lerbs, Savita Bisht, Sebastian Schölch, Mathieu Pecqueux, Glen Kristiansen, Martin Schneider, Bianca T Hofmann, Thilo Welsch, Christoph Reissfelder, Nuh N Rahbari and 5 more

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

22 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
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  5. Article
  6. Article
  7. SIX1 Downregulation Suppresses Self-renewal Capacity and THY1 Expression in Hepatocellular Carcinoma and SIX1 Dominate the Survival in Liver Cancer.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2023
    Article
  8. Article
  9. Review
  10. Article
  11. The Role of CDK4 in the Pathogenesis of Pancreatic Cancer.Healthcare (Basel, Switzerland) · 2021
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
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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

15 authors at 3 institutions in 1 country.

Tristan LerbsDepartment of General, Visceral and Transplantation Surgery, Im Neuenheimer Feld 110, 69120, Heidelberg, Germany.
Savita BishtDepartment of Internal Medicine 3, Center of Integrated Oncology (CIO) Cologne-Bonn, University Hospital of Bonn, Bonn, Germany.
Sebastian SchölchDepartment of Gastrointestinal, Thoracic and Vascular Surgery, Medizinische Fakultät Carl Gustav Carus, Technische Universität Dresden, Fetscherstr. 74, 01307, Dresden, Germany.
Mathieu PecqueuxDepartment of Gastrointestinal, Thoracic and Vascular Surgery, Medizinische Fakultät Carl Gustav Carus, Technische Universität Dresden, Fetscherstr. 74, 01307, Dresden, Germany.
Glen KristiansenDepartment of Pathology, Center of Integrated Oncology Cologne-Bonn, University Hospital of Bonn, Bonn, Germany.
Martin SchneiderDepartment of General, Visceral and Transplantation Surgery, Im Neuenheimer Feld 110, 69120, Heidelberg, Germany.
Bianca T HofmannDepartment of General, Visceral and Thoracic Surgery, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, 20246, Hamburg, Germany.
Thilo WelschDepartment of Gastrointestinal, Thoracic and Vascular Surgery, Medizinische Fakultät Carl Gustav Carus, Technische Universität Dresden, Fetscherstr. 74, 01307, Dresden, Germany.
Christoph ReissfelderDepartment of Gastrointestinal, Thoracic and Vascular Surgery, Medizinische Fakultät Carl Gustav Carus, Technische Universität Dresden, Fetscherstr. 74, 01307, Dresden, Germany.
Nuh N RahbariDepartment of Gastrointestinal, Thoracic and Vascular Surgery, Medizinische Fakultät Carl Gustav Carus, Technische Universität Dresden, Fetscherstr. 74, 01307, Dresden, Germany.
Johannes FritzmannDepartment of Gastrointestinal, Thoracic and Vascular Surgery, Medizinische Fakultät Carl Gustav Carus, Technische Universität Dresden, Fetscherstr. 74, 01307, Dresden, Germany.
Peter BrossartDepartment of Internal Medicine 3, Center of Integrated Oncology (CIO) Cologne-Bonn, University Hospital of Bonn, Bonn, Germany.
Jürgen WeitzDepartment of Gastrointestinal, Thoracic and Vascular Surgery, Medizinische Fakultät Carl Gustav Carus, Technische Universität Dresden, Fetscherstr. 74, 01307, Dresden, Germany.
Georg FeldmannDepartment of Internal Medicine 3, Center of Integrated Oncology (CIO) Cologne-Bonn, University Hospital of Bonn, Bonn, Germany.
Christoph KahlertDepartment of General, Visceral and Transplantation Surgery, Im Neuenheimer Feld 110, 69120, Heidelberg, Germany. christoph.kahlert.079@googlemail.com.
TU Dresden · DEUniversity Hospital Bonn · DEUniversität Hamburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEpithelial-to-mesenchymal transition (EMT) and cancer stem cells (CSC) contribute to tumour progression and metastasis. Assessment of transcription factors involved in these two mechanisms can help to identify new targets for an oncological therapy. In this study, we focused on the evaluation of the transcription factor Six1 (Sine oculis 1). This protein is involved in embryologic development and its contribution to carcinogenesis has been described in several studies.

methodsImmunohistochemistry against Six1 was performed on a tissue microarray containing specimens of primary pancreatic ductal adenocarcinomas (PDAC) of 139 patients. Nuclear and cytoplasmic expression was evaluated and correlated to histopathological parameters. Expression of Six1 was inhibited transiently by siRNA in Panc1 and BxPc3 cells and stably by shRNA in Panc1 cells. Expression analysis of CDH1 and Vimentin mRNA was performed and cell motility was tested in a migration assay. Panc1 cells transfected with Six1 shRNA or scrambled shRNA were injected subcutaneously into nude mice. Tumour growth was observed for four weeks. Afterwards, tumours were stained against Six1, CD24 and CD44.

resultsSix1 was overexpressed in the cytoplasm and cellular nuclei in malignant tissues (p < 0.0001). No correlation to histopathological parameters could be detected. Six1 down-regulation decreased pancreatic cancer cell motility in vitro. CDH1 and vimentin expression was decreased after inhibition of the expression of Six1. Pancreatic tumours with impaired expression of Six1 showed significantly delayed growth and displayed loss of the CD24

conclusionWe show that Six1 is overexpressed in human PDAC and that its inhibition results in a decreased tumour progression in vitro and in vivo. Therefore, targeting Six1 might be a novel therapeutic approach in patients with pancreatic cancer.

Indexed as

Gene Expression Regulation, NeoplasticRNA InterferenceAnimalsEpithelial-Mesenchymal TransitionHomeodomain ProteinsHumansMiceMice, NudeNeoplasm InvasivenessNeoplastic Stem CellsPancreatic NeoplasmsXenograft Model Antitumor AssaysHomeodomain ProteinsSIX1 protein, humanCancer stem cellsEpithelial-mesenchymal transitionPancreatic cancerSix1

Identifiers

PMID28388884
PMCPMC5383957
OpenAlexW2604137159

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.