Evidence map›Paper›PMID 22900040›Full record

ArticlePloS one2012

Overexpressed galectin-3 in pancreatic cancer induces cell proliferation and invasion by binding Ras and activating Ras signaling.

Shumei Song, Baoan Ji, Vijaya Ramachandran, Huamin Wang, Margarete Hafley, Craig Logsdon, Robert S Bresalier

Abstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
–field-weighted citation impact
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

71 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. The Role of Glycans in Human Immunity-A Sweet Code.Molecules (Basel, Switzerland) · 2025
    Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. The immune response to a fungus in pancreatic cancer samples.bioRxiv : the preprint server for biology · 2023
    Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Cancers · 2022
    Article
  19. Article
  20. Human umbilical cord mesenchymal stem cell-derived exosomes carrying hsa-miRNA-128-3p suppress pancreatic ductal cell carcinoma by inhibiting Galectin-3.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    Article

11 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

7 authors.

Shumei SongDepartment of Gastroenterology, Hepatology, and Nutrition, University of Texas MD Anderson Cancer Center, Houston, Texas, United States of America. ssong@mdanderson.org
Baoan Ji
Vijaya Ramachandran
Huamin Wang
Margarete Hafley
Craig Logsdon
Robert S Bresalier

Funding

MOLECULAR MECHANISMS OF PANCREATITISR01DK052067 · NIDDK · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LOGSDON, CRAIG D · 1998 to 2015
$4.4M
MUCIN GLYCOPROTEINS IN COLON CANCER METASTASISR01CA069480 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BRESALIER, ROBERT S · 1996 to 2010
$2.6M
NCI NIH HHS R01 CA069480NCI NIH HHS R01CA69480NIDDK NIH HHS R01 DK052067PHS HHS DF56338
6 · The paper itself

Abstract

Pancreatic cancer (PDAC) is a lethal disease with a five-year survival of 3-5%. Mutations in K-Ras are found in nearly all cases, but K-Ras mutations alone are not sufficient for the development of PDAC. Additional factors contribute to activation of Ras signaling and lead to tumor formation. Galectin-3 (Gal-3), a multifunctional β-galactoside-binding protein, is highly expressed in PDAC. We therefore investigated the functional role of Gal-3 in pancreatic cancer progression and its relationship to Ras signaling. Expression of Gal-3 was determined by immunohistochemistry, Q-PCR and immunoblot. Functional studies were performed using pancreatic cell lines genetically engineered to express high or low levels of Gal-3. Ras activity was examined by Raf pull-down assays. Co-immunoprecipitation and immunofluorescence were used to assess protein-protein interactions. In this study, we demonstrate that Gal-3 was highly up-regulated in human tumors and in a mutant K-Ras mouse model of PDAC. Down-regulation of Gal-3 by lentivirus shRNA decreased PDAC cell proliferation and invasion in vitro and reduced tumor volume and size in an orthotopic mouse model. Gal-3 bound Ras and maintained Ras activity; down-regulation of Gal-3 decreased Ras activity as well as Ras down-stream signaling including phosphorylation of ERK and AKT and Ral A activity. Transfection of Gal-3 cDNA into PDAC cells with low-level Gal-3 augmented Ras activity and its down-stream signaling. These results suggest that Gal-3 contributes to pancreatic cancer progression, in part, by binding Ras and activating Ras signaling. Gal-3 may therefore be a potential novel target for this deadly disease.

Indexed as

Gene ExpressionSignal TransductionAnimalsCarcinoma, Pancreatic DuctalCell Line, TumorCell ProliferationGalectin 3Gene Expression Regulation, NeoplasticHumansMiceMutationNeoplasm InvasivenessPancreatic NeoplasmsProtein Bindingras ProteinsRNA InterferenceGalectin 3ras Proteins

Identifiers

PMID22900040
PMCPMC3416861

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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.