Evidence map›Paper›PMID 27391068›Full record

ArticleOncotarget2017

Loss of LSR affects epithelial barrier integrity and tumor xenograft growth of CaCo-2 cells.

Bernd A Czulkies, Justin Mastroianni, Lisa Lutz, Sarah Lang, Carsten Schwan, Gudula Schmidt, Silke Lassmann, Robert Zeiser, Klaus Aktories, Panagiotis Papatheodorou

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

15 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. LSR Promotes Cell Proliferation and Invasion in Lung Cancer.Computational and mathematical methods in medicine · 2021
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Mutations in theProceedings of the National Academy of Sciences of the United States of America · 2018
    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

10 authors at 4 institutions in 1 country.

Bernd A CzulkiesInstitute of Experimental and Clinical Pharmacology and Toxicology, Albert-Ludwigs-University (ALU), Freiburg, Germany.
Justin MastroianniDepartment of Hematology and Oncology, University Medical Center, ALU, Freiburg, Germany.
Lisa LutzDepartment of Pathology, University Medical Center, ALU, Freiburg, Germany.
Sarah LangInstitute of Experimental and Clinical Pharmacology and Toxicology, Albert-Ludwigs-University (ALU), Freiburg, Germany.
Carsten SchwanInstitute of Experimental and Clinical Pharmacology and Toxicology, Albert-Ludwigs-University (ALU), Freiburg, Germany.
Gudula SchmidtInstitute of Experimental and Clinical Pharmacology and Toxicology, Albert-Ludwigs-University (ALU), Freiburg, Germany.
Silke LassmannDepartment of Pathology, University Medical Center, ALU, Freiburg, Germany.
Robert ZeiserDepartment of Hematology and Oncology, University Medical Center, ALU, Freiburg, Germany.
Klaus AktoriesInstitute of Experimental and Clinical Pharmacology and Toxicology, Albert-Ludwigs-University (ALU), Freiburg, Germany.
Panagiotis PapatheodorouInstitute of Experimental and Clinical Pharmacology and Toxicology, Albert-Ludwigs-University (ALU), Freiburg, Germany.
University of Freiburg · DEUniversity Medical Center Freiburg · DEHeidelberg University · DEUniversität Ulm · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The lipolysis-stimulated lipoprotein receptor (LSR) is a lipoprotein receptor, serves as host receptor for clostridial iota-like toxins and is involved in the formation of tricellular contacts. Of particular interest is the role of LSR in progression of various cancers. Here we aimed to study the tumor growth of LSR-deficient colon carcinoma-derived cell lines HCT116 and CaCo-2 in a mouse xenograft model. Whereas knockout of LSR had no effect on tumor growth of HCT116 cells, we observed that CaCo-2 LSR knockout tumors grew to a smaller size than their wild-type counterparts. Histological analysis revealed increased apoptotic and necrotic cell death in a tumor originating from LSR-deficient CaCo-2 cells. LSR-deficient CaCo-2 cells exhibited increased cell proliferation in vitro and an altered epithelial morphology with impaired targeting of tricellulin to tricellular contacts. In addition, loss of LSR reduced the transepithelial electrical resistance of CaCo-2 cell monolayers and increased permeability for small molecules. Moreover, LSR-deficient CaCo-2 cells formed larger cysts in 3D culture than their wild-type counterparts. Our study provides evidence that LSR affects epithelial morphology and barrier formation in CaCo-2 cells and examines for the first time the effects of LSR deficiency on the tumor growth properties of colon carcinoma-derived cell lines.

Indexed as

Cell Membrane PermeabilityAnimalsBase SequenceCaco-2 CellsCell ProliferationColonic NeoplasmsEpithelial CellsGene Knockout TechniquesHCT116 CellsHumansMaleMice, Inbred BALB CMice, KnockoutMice, NudeReceptors, LipoproteinTransplantation, HeterologousReceptors, Lipoproteincell-cell contactcell morphologyepithelial barriertumor growthxenograft

Identifiers

PMID27391068
PMCPMC5514888
OpenAlexW2464755258

What OpenQuestion 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 OpenQuestion graph.