Evidence map›Paper›PMID 25125675›Full record

ArticleMolecular cancer therapeutics2014

Inhibition of endoglin-GIPC interaction inhibits pancreatic cancer cell growth.

Krishnendu Pal, Alexandre A Pletnev, Shamit K Dutta, Enfeng Wang, Ruizhi Zhao, Aradhita Baral, Vinod Kumar Yadav, Suruchi Aggarwal, Soundararajan Krishnaswamy, Khalid M Alkharfy and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer therapeutics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Endoglin in the Spotlight to Treat Cancer.International journal of molecular sciences · 2021
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. 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

13 authors at 4 institutions in 3 countries.

Krishnendu PalDepartment of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota.
Alexandre A PletnevDepartment of Pharmacology and Toxicology, Geisel School of Medicine at Dartmouth and Norris Cotton Cancer Center, Lebanon, New Hampshire.
Shamit K DuttaDepartment of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota.
Enfeng WangDepartment of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota.
Ruizhi ZhaoDepartment of Pharmacology and Toxicology, Geisel School of Medicine at Dartmouth and Norris Cotton Cancer Center, Lebanon, New Hampshire.
Aradhita BaralProteomics and Structural Biology Unit, Institute of Genomics and Integrative Biology, Council for Scientific and Industrial Research, New Delhi, India.
Vinod Kumar YadavG.N.R. Knowledge Center for Genome Informatics, Institute of Genomics and Integrative Biology, Council for Scientific and Industrial Research, New Delhi, India.
Suruchi AggarwalG.N.R. Knowledge Center for Genome Informatics, Institute of Genomics and Integrative Biology, Council for Scientific and Industrial Research, New Delhi, India.
Soundararajan KrishnaswamyDepartment of Biochemistry, King Saud University, Riyadh, Saudi Arabia.
Khalid M AlkharfyDepartment of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota. Department of Pharmacy, King Saud University, Riyadh, Saudi Arabia.
Shantanu ChowdhuryProteomics and Structural Biology Unit, Institute of Genomics and Integrative Biology, Council for Scientific and Industrial Research, New Delhi, India. G.N.R. Knowledge Center for Genome Informatics, Institute of Genomics and Integrative Biology, Council for Scientific and Industrial Research, New Delhi, India.
Mark R SpallerDepartment of Pharmacology and Toxicology, Geisel School of Medicine at Dartmouth and Norris Cotton Cancer Center, Lebanon, New Hampshire.
Debabrata MukhopadhyayDepartment of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota. mukhopadhyay.debabrata@mayo.edu.
Mayo Clinic · USInstitute of Genomics and Integrative Biology · INDartmouth College · USKing Saud University · SA

Funding

Targeting Pancreatic Cancer Using Peptide Chemistry: From Bench to BedsideR01CA150190 · NCI · MAYO CLINIC ROCHESTER · PI MIERKE, DALE F, MUKHOPADHYAY, DEBABRATA · 2010 to 2021
$5.7M
Regulatory Pathways and Role of VPF/VEGF in Renal CancerR01CA078383 · NCI · MAYO CLINIC ROCHESTER · PI MUKHOPADHYAY, DEBABRATA · 2004 to 2019
$4.5M
REGULATORY PATHWAYS AND ROLE OF VPF/VEGF IN RENAL CANCERR29CA078383 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI MUKHOPADHYAY, DEBABRATA · 1998 to 2002
$383k
NCI NIH HHS CA150190NCI NIH HHS CA78383NCI NIH HHS R01 CA078383NCI NIH HHS R01 CA150190NCI NIH HHS R29 CA078383
6 · The paper itself

Abstract

Endoglin, a 180-kDa disulfide-linked homodimeric transmembrane receptor protein mostly expressed in tumor-associated endothelial cells, is an endogenous binding partner of GAIP-interacting protein, C terminus (GIPC). Endoglin functions as a coreceptor of TβRII that binds TGFβ and is important for vascular development, and consequently has become a compelling target for antiangiogenic therapies. A few recent studies in gastrointestinal stromal tumor (GIST), breast cancer, and ovarian cancer, however, suggest that endoglin is upregulated in tumor cells and is associated with poor prognosis. These findings indicate a broader role of endoglin in tumor biology, beyond angiogenic effects. The goal of our current study is to evaluate the effects of targeting endoglin in pancreatic cancer both in vitro and in vivo. We analyzed the antiproliferative effect of both RNAi-based and peptide ligand-based inhibition of endoglin in pancreatic cancer cell lines, the latter yielding a GIPC PDZ domain-targeting lipopeptide with notable antiproliferative activity. We further demonstrated that endoglin inhibition induced a differentiation phenotype in the pancreatic cancer cells and sensitized them against conventional chemotherapeutic drug gemcitabine. Most importantly, we have demonstrated the antitumor effect of both RNAi-based and competitive inhibitor-based blocking of endoglin in pancreatic cancer xenograft models in vivo. To our knowledge, this is the first report exploring the effect of targeting endoglin in pancreatic cancer cells.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsAntigens, CDCell Growth ProcessesCell Line, TumorDeoxycytidineDrug SynergismEndoglinGemcitabineHumansLigandsMaleMiceMice, SCIDMolecular Targeted TherapyPancreatic NeoplasmsAdaptor Proteins, Signal TransducingAntigens, CDDeoxycytidineEndoglinENG protein, humanGemcitabineGIPC1 protein, humanLigandsPeptidesReceptors, Cell SurfaceRNA, Small Interfering

Identifiers

PMID25125675
PMCPMC4229952
OpenAlexW2154758303

What OpenQuestion holds

Textmetadata
LicenceTDM
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.