Evidence map›Paper›PMID 19028702›Full record

ArticleCarcinogenesis2009

Aberrant activation of hedgehog signaling pathway in ovarian cancers: effect on prognosis, cell invasion and differentiation.

Xiaoyun Liao, Michelle K Y Siu, Christy W H Au, Esther S Y Wong, Hoi Yan Chan, Philip P C Ip, Hextan Y S Ngan, Annie N Y Cheung

Open access · bronzeAbstract read
In one paragraph

Article in Carcinogenesis, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
126citing papers in PubMed, 3 pooled it
4.7field-weighted citation impact, top 4% 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

126 citing papers in PubMed, 3 syntheses or guidelines pooled it, 197 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Article
  6. Review
  7. Review
  8. The Prognostic Value of the Hedgehog Signaling Pathway in Ovarian Cancer.International journal of molecular sciences · 2025
    Article
  9. Article
  10. GPR137-RAB8A activation promotes ovarian cancer development via the Hedgehog pathway.Journal of experimental & clinical cancer research : CR · 2025
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. MYCN in human development and diseases.Frontiers in oncology · 2024
    Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

66 more citing papers are in PubMed but not listed here.

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

8 authors at 2 institutions in 2 countries.

Xiaoyun LiaoDepartment of Pathology, The University of Hong Kong, Queen Mary Hospital, Pokfulam, Hong Kong, China.
Michelle K Y Siu
Christy W H Au
Esther S Y Wong
Hoi Yan Chan
Philip P C Ip
Hextan Y S Ngan
Annie N Y Cheung
Queen Mary Hospital · CNUniversity of Hong Kong · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aberrant activation of hedgehog (HH) pathway has been implicated in the development of human malignancies. This study aimed at investigating the role of HH molecules in human ovarian carcinogenesis. The expression profiles of HH molecules were examined in ovarian tumor samples and ovarian cancer cell lines and the in vitro effects of HH molecules on cell proliferation, apoptosis, migration, invasion and cell differentiation as well as related downstream target genes were assessed. Overexpression of Patched and Gli1 protein in ovarian cancers correlated with poor survival of the patients (P = 0.008; P = 0.004). Significantly elevated expression of Sonic hedgehog messenger RNA was observed in ovarian cancers compared with normal tissues and benign ovarian tumors and such differential expression was specific to histological types (P < 0.05). Ectopic Gli1 overexpression in ovarian cancer cells conferred increased cell proliferation, cell mobility, invasiveness and change in differentiation in association with increased expression of E-cadherin, vimentin, Bcl-2, caspases as well as beta1 integrin, membrane type 1 matrix metalloproteinase (MT1-MMP) and vascular endothelial growth factor (VEGF). Treatment with 3-keto-N-(aminoethyl-aminocaproyl-dihydrocinnamoyl)-cyclopamine induced cancer cell apoptosis, suppressed cell growth, mobility and invasiveness and induced cancer cell dedifferentiation with decreased expression of E-cadherin, cytokeratin 7, Snail, calretinin, vimentin, Bcl-2, caspases, beta1 integrin, MT1-MMP and VEGF. Our data suggested that abnormal HH signaling activation plays important roles in the development and progression of ovarian cancers. Gli1 expression is an independent prognostic marker. Inhibition of the HH pathway molecules might be a valid therapeutic strategy for ovarian cancers.

Indexed as

Cell DifferentiationNeoplasm InvasivenessSignal TransductionCell Line, TumorFemaleHedgehog ProteinsHumansImmunohistochemistryOvarian NeoplasmsPatched ReceptorsPrognosisReceptors, Cell SurfaceReverse Transcriptase Polymerase Chain ReactionTranscription FactorsZinc Finger Protein GLI1GLI1 protein, humanHedgehog ProteinsPatched ReceptorsReceptors, Cell SurfaceTranscription FactorsZinc Finger Protein GLI1

Identifiers

PMID19028702
PMCPMC7109814
OpenAlexW2145447734

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.