Evidence map›Paper›PMID 27872089›Full record

ArticleCancer research2017

Transcriptional Induction of Periostin by a Sulfatase 2-TGFβ1-SMAD Signaling Axis Mediates Tumor Angiogenesis in Hepatocellular Carcinoma.

Gang Chen, Ikuo Nakamura, Renumathy Dhanasekaran, Eriko Iguchi, Ezequiel J Tolosa, Paola A Romecin, Renzo E Vera, Luciana L Almada, Alexander G Miamen, Roongruedee Chaiteerakij and 20 more

Open access · hybridAbstract read
In one paragraph

Article in Cancer research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Review
  6. Monocyte-derived exosomal periostin driven by histone lactylation contributes to retinal neovascularization.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Loss of DNA Polymerase β Delays Atherosclerosis inInternational journal of molecular sciences · 2024
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Periostin: an emerging activator of multiple signaling pathways.Journal of cell communication and signaling · 2022
    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

30 authors at 5 institutions in 4 countries.

Gang ChenDivision of Hepatobiliary Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China.
Ikuo NakamuraDivision of Gastroenterology and Hepatology, Mayo Clinic College of Medicine and Science, Rochester, Minnesota.
Renumathy DhanasekaranDivision of Gastroenterology and Hepatology, Mayo Clinic College of Medicine and Science, Rochester, Minnesota.
Eriko IguchiSchulze Center for Novel Therapeutics, Mayo Clinic, Rochester, Minnesota.
Ezequiel J TolosaSchulze Center for Novel Therapeutics, Mayo Clinic, Rochester, Minnesota.
Paola A RomecinSchulze Center for Novel Therapeutics, Mayo Clinic, Rochester, Minnesota.
Renzo E VeraSchulze Center for Novel Therapeutics, Mayo Clinic, Rochester, Minnesota.
Luciana L AlmadaSchulze Center for Novel Therapeutics, Mayo Clinic, Rochester, Minnesota.
Alexander G MiamenDivision of Gastroenterology and Hepatology, Mayo Clinic College of Medicine and Science, Rochester, Minnesota.
Roongruedee ChaiteerakijDivision of Gastroenterology and Hepatology, Mayo Clinic College of Medicine and Science, Rochester, Minnesota.
Mengtao ZhouDivision of Hepatobiliary Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China.
Michael K AsieduDivision of Gastroenterology and Hepatology, Mayo Clinic College of Medicine and Science, Rochester, Minnesota.
Catherine D MoserDivision of Gastroenterology and Hepatology, Mayo Clinic College of Medicine and Science, Rochester, Minnesota.
Shaoshan HanDivision of Gastroenterology and Hepatology, Mayo Clinic College of Medicine and Science, Rochester, Minnesota.
Chunling HuDivision of Gastroenterology and Hepatology, Mayo Clinic College of Medicine and Science, Rochester, Minnesota.
Bubu A BaniniDivision of Gastroenterology and Hepatology, Mayo Clinic College of Medicine and Science, Rochester, Minnesota.
Abdul M OseiniDivision of Gastroenterology and Hepatology, Mayo Clinic College of Medicine and Science, Rochester, Minnesota.
Yichun ChenDivision of Gastroenterology and Hepatology, Mayo Clinic College of Medicine and Science, Rochester, Minnesota.
Yong FangDivision of Gastroenterology and Hepatology, Mayo Clinic College of Medicine and Science, Rochester, Minnesota.
Dongye YangDivision of Gastroenterology and Hepatology, Mayo Clinic College of Medicine and Science, Rochester, Minnesota.
Hassan M ShalehDivision of Gastroenterology and Hepatology, Mayo Clinic College of Medicine and Science, Rochester, Minnesota.
Shaoqing WangDivision of Gastroenterology and Hepatology, Mayo Clinic College of Medicine and Science, Rochester, Minnesota.
Dehai WuDivision of Gastroenterology and Hepatology, Mayo Clinic College of Medicine and Science, Rochester, Minnesota.
Tao SongDivision of Gastroenterology and Hepatology, Mayo Clinic College of Medicine and Science, Rochester, Minnesota.
Ju-Seog LeeDepartment of Systems Biology, MD Anderson Cancer Center, Houston, Texas.
Snorri S ThorgeirssonLaboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, Maryland.
Eric ChevetINSERM U1242, Chemistry, Oncogenesis Stress Signaling, Université Rennes 1, and Centre de Lutte Contre le Cancer Eugène Marquis, Rennes, France.
Vijay H ShahDivision of Gastroenterology and Hepatology, Mayo Clinic College of Medicine and Science, Rochester, Minnesota.
Martin E Fernandez-ZapicoDivision of Gastroenterology and Hepatology, Mayo Clinic College of Medicine and Science, Rochester, Minnesota.
Lewis R RobertsDivision of Gastroenterology and Hepatology, Mayo Clinic College of Medicine and Science, Rochester, Minnesota. roberts.lewis@mayo.edu.
Mayo Clinic · USInserm · FRNational Cancer Institute · USThe University of Texas MD Anderson Cancer Center · USWenzhou Medical University · CN

Funding

Women's Cancer ProgramP30CA015083 · NCI · MAYO CLINIC ROCHESTER · PI Felicity Enders · 1985 to 2026
$151.3M
Mayo Clinic Center for Translational Science ActivitiesUL1TR000135 · NCATS · MAYO CLINIC ROCHESTER · PI KHOSLA, SUNDEEP · 2012 to 2015
$41.2M
PILOT AND FEASIBILTY PROGRAMP30DK084567 · NIDDK · MAYO CLINIC ROCHESTER · PI GREGORY J. GORES · 2009 to 2026
$22.2M
Regulation of the Tumor Microenvironment in Hepatocellular CarcinomaR01CA165076 · NCI · MAYO CLINIC ROCHESTER · PI FERNANDEZ-ZAPICO, MARTIN ERNESTO, ROBERTS, LEWIS R · 2012 to 2016
$2.0M
Dysregulation of the Tumor Microenvironment in Hepatocellular CarcinomaR21CA128633 · NCI · MAYO CLINIC ROCHESTER · PI ROBERTS, LEWIS R · 2009 to 2010
$366k
NCATS NIH HHS UL1 TR000135NCI NIH HHS N01 CA015083NCI NIH HHS P30 CA015083NCI NIH HHS R01 CA165076NCI NIH HHS R21 CA128633NIDDK NIH HHS P30 DK084567
6 · The paper itself

Abstract

Existing antiangiogenic approaches to treat metastatic hepatocellular carcinoma (HCC) are weakly effectual, prompting further study of tumor angiogenesis in this disease setting. Here, we report a novel role for sulfatase 2 (SULF2) in driving HCC angiogenesis. Sulf2-deficient mice (Sulf2 KO) exhibited resistance to diethylnitrosamine-induced HCC and did not develop metastases like wild-type mice (Sulf2 WT). The smaller and less numerous tumors formed in Sulf2 KO mice exhibited a markedly lower microvascular density. In human HCC cells, SULF2 overexpression increased endothelial proliferation, adhesion, chemotaxis, and tube formation in a paracrine fashion. Mechanistic analyses identified the extracellular matrix protein periostin (POSTN), a ligand of αvβ3/5 integrins, as an effector protein in SULF2-induced angiogenesis. POSTN silencing in HCC cells attenuated SULF2-induced angiogenesis and tumor growth in vivo The TGFβ1/SMAD pathway was identified as a critical signaling axis between SULF2 and upregulation of POSTN transcription. In clinical HCC specimens, elevated levels of SULF2 correlated with increased microvascular density, POSTN levels, and relatively poorer patient survival. Together, our findings define an important axis controlling angiogenesis in HCC and a mechanistic foundation for rational drug development. Cancer Res; 77(3); 632-45. ©2016 AACR.

Indexed as

AnimalsBiomarkers, TumorBlotting, WesternCarcinoma, HepatocellularCell Adhesion MoleculesChromatin ImmunoprecipitationEnzyme-Linked Immunosorbent AssayGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansImmunohistochemistryKaplan-Meier EstimateLiver NeoplasmsMiceMice, KnockoutNeovascularization, PathologicBiomarkers, TumorCell Adhesion MoleculesPOSTN protein, humanSmad ProteinsSULF2 protein, humanSulfatasesSulfotransferasesTransforming Growth Factor beta1

Identifiers

PMID27872089
PMCPMC5429157
OpenAlexW2551798322

What OpenQuestion holds

Textmetadata
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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.