Evidence map›Paper›PMID 27323403›Full record

SynthesisOncotarget2016

FH535, a β-catenin pathway inhibitor, represses pancreatic cancer xenograft growth and angiogenesis.

Lu Liu, Qiaoming Zhi, Meng Shen, Fei-Ran Gong, Binhua P Zhou, Lian Lian, Bairong Shen, Kai Chen, Weiming Duan, Meng-Yao Wu and 2 more

Open access · diamondAbstract readMeta-Analysis
In one paragraph

Synthesis in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.4field-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

19 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
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  3. Review
  4. Review
  5. Article
  6. Effects of the Wnt/Contrast media & molecular imaging · 2022
    Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
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  15. Article
  16. Eradicating Cancer Stem Cells: Concepts, Issues, and Challenges.Current treatment options in oncology · 2018
    Review
  17. Article
  18. Article
  19. 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

12 authors at 3 institutions in 2 countries.

Lu LiuDepartment of Oncology, The First Affiliated Hospital of Soochow University, Suzhou, China.
Qiaoming ZhiDepartment of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou, China.
Meng ShenDepartment of Oncology, The First Affiliated Hospital of Soochow University, Suzhou, China.
Fei-Ran GongDepartment of Hematology, The First Affiliated Hospital of Soochow University, Suzhou, China.
Binhua P ZhouMarkey Cancer Center, University of Kentucky, Lexington, KY, USA.
Lian LianDepartment of Oncology, The First Affiliated Hospital of Soochow University, Suzhou, China.
Bairong ShenCenter for Systems Biology, Soochow University, Suzhou, China.
Kai ChenDepartment of Oncology, The First Affiliated Hospital of Soochow University, Suzhou, China.
Weiming DuanDepartment of Oncology, The First Affiliated Hospital of Soochow University, Suzhou, China.
Meng-Yao WuDepartment of Oncology, The First Affiliated Hospital of Soochow University, Suzhou, China.
Min TaoDepartment of Oncology, The First Affiliated Hospital of Soochow University, Suzhou, China.
Wei LiDepartment of Oncology, The First Affiliated Hospital of Soochow University, Suzhou, China.
Soochow University · CNFirst Affiliated Hospital of Soochow University · CNMarkey Cancer Center · US

Funding

University of Kentucky Markey Cancer Center Support Grant ECIA SupplementP30CA177558 · NCI · UNIVERSITY OF KENTUCKY · PI Jennifer F Rogers · 2013 to 2026
$38.3M
NCI NIH HHS P30 CA177558
6 · The paper itself

Abstract

The WNT/β-catenin pathway plays an important role in pancreatic cancer carcinogenesis. We evaluated the correlation between aberrant β-catenin pathway activation and the prognosis pancreatic cancer, and the potential of applying the β-catenin pathway inhibitor FH535 to pancreatic cancer treatment. Meta-analysis and immunohistochemistry showed that abnormal β-catenin pathway activation was associated with unfavorable outcome. FH535 repressed pancreatic cancer xenograft growth in vivo. Gene Ontology (GO) analysis of microarray data indicated that target genes responding to FH535 participated in stemness maintenance. Real-time PCR and flow cytometry confirmed that FH535 downregulated CD24 and CD44, pancreatic cancer stem cell (CSC) markers, suggesting FH535 impairs pancreatic CSC stemness. GO analysis of β-catenin chromatin immunoprecipitation sequencing data identified angiogenesis-related gene regulation. Immunohistochemistry showed that higher microvessel density correlated with elevated nuclear β-catenin expression and unfavorable outcome. FH535 repressed the secretion of the proangiogenic cytokines vascular endothelial growth factor (VEGF), interleukin (IL)-6, IL-8, and tumor necrosis factor-α, and also inhibited angiogenesis in vitro and in vivo. Protein and mRNA microarrays revealed that FH535 downregulated the proangiogenic genes ANGPT2, VEGFR3, IFN-γ, PLAUR, THPO, TIMP1, and VEGF. FH535 not only represses pancreatic CSC stemness in vitro, but also remodels the tumor microenvironment by repressing angiogenesis, warranting further clinical investigation.

Indexed as

beta CateninCell Growth ProcessesCell Line, TumorFemaleHumansNeovascularization, PathologicPancreatic NeoplasmsSulfonamidesTransfectionXenograft Model Antitumor Assaysbeta CateninFH535Sulfonamidesangiogenesiscancer stem cellFH535pancreatic cancerβ-catenin

Identifiers

PMID27323403
PMCPMC5216931
OpenAlexW2442495408

What Socratic 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 Socratic graph.