Evidence map›Paper›PMID 20459627›Full record

ArticleBMC cancer2010

Adhesion of renal carcinoma cells to endothelial cells depends on PKCmu.

Walburgis Brenner, Silke Beitz, Elke Schneider, Frank Benzing, Ronald E Unger, Frederik C Roos, Joachim W Thüroff, Christian Hampel

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.5field-weighted citation impact, top 38% 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

11 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Lysophosphatidic acid enhances breast cancer cells-mediated osteoclastogenesis.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2018
    Article
  5. Article
  6. Protein kinase D signaling in cancer: A friend or foe?Biochimica et biophysica acta. Reviews on cancer · 2017
    Review
  7. Article
  8. Article
  9. Article
  10. Emerging roles of protein kinase D1 in cancer.Molecular cancer research : MCR · 2011
    Review
  11. 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

8 authors at 2 institutions in 1 country.

Walburgis BrennerDepartment of Urology, University Medical Center Mainz, Mainz, Germany. brenner@uni-mainz.de
Silke Beitz
Elke Schneider
Frank Benzing
Ronald E Unger
Frederik C Roos
Joachim W Thüroff
Christian Hampel
University Medical Center of the Johannes Gutenberg University Mainz · DEJohannes Gutenberg University Mainz · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe formation of metastases includes the separation of tumor cells from the primary tumor, cell migration into subendothelial tissue and cell proliferation in secondary organ. In this process, cell adhesion of tumor cells to the endothelium is an essential requirement for formation of metastases. Protein kinase C (PKC) regulates adhesion and proliferation. To identify a relation between PKC isoforms and tumor progression in renal cell carcinoma (RCC), the influence of PKC isoforms on cell adhesion and proliferation, and possible influences of integrins were analyzed in RCC cells.

methodsThe experiments were performed in the RCC cell lines CCF-RC1 and CCF-RC2 after pre-incubation (16 h) with the PKC inhibitors GF109203X (inhibits PKCalpha, betaI, betaII, gamma, delta and epsilon), GO6976 (inhibits PKCalpha, betaI and mu), RO31-8220 (inhibits PKCalpha, betaI, betaII, gamma and epsilon) and rottlerin (inhibits PKCdelta). Cell adhesion was assessed through adherence of RCC cells to an endothelial monolayer. Cell proliferation was analyzed by a BrdU incorporation assay. The expression of beta1 integrins was analyzed by flow cytometry.

resultsIn CCF-RC1 cells, cell adhesion was significantly reduced by GO6976 to 55% and by RO31-8220 to 45% of control. In CCF-RC2 cells, only GO6976 induced a significant reduction of cell adhesion to 50% of control levels. Proliferation of both cell lines was reduced by rottlerin to 39% and 45% of control, respectively. The beta1 integrin expression on the cell surface of CCF-RC1 and CCR-RC2 cells was decreased by RO31-8220 to 8% and 7% of control, respectively. beta2 and beta3 integrins were undetectable in both cell lines.

conclusionsThe combination of the PKC inhibitors leads to the assumption that PKCmu influences cell adhesion in CCF-RC1 and CCF-RC2 cells, whereas in CCF-RC1 cells PKCepsilon also seems to be involved in this process. The expression of beta1 integrins appears to be regulated in particular by PKCepsilon. Cell proliferation was inhibited by rottlerin, so that PKCdelta might be involved in cell proliferation in these cells.

Indexed as

Carcinoma, Renal CellCell AdhesionCell Growth ProcessesCell Line, TumorEndothelial CellsHumansIntegrin beta ChainsKidney NeoplasmsProtein Kinase CProtein Kinase InhibitorsIntegrin beta ChainsProtein Kinase Cprotein kinase DProtein Kinase Inhibitors

Identifiers

PMID20459627
PMCPMC2873397
OpenAlexW2060052894

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.