Evidence map›Paper›PMID 19194507›Full record

ArticlePloS one2009

Tensin3 is a negative regulator of cell migration and all four Tensin family members are downregulated in human kidney cancer.

Danuta Martuszewska, Börje Ljungberg, Martin Johansson, Göran Landberg, Cecilia Oslakovic, Björn Dahlbäck, Sassan Hafizi

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 18% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Identification of Tensin-3 as a MALT1 substrate that controls B cell adhesion and lymphoma dissemination.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  6. Article
  7. The molecular and clinical role of Tensin 1/2/3 in cancer.Journal of cellular and molecular medicine · 2023
    Review
  8. Tensins in Kidney Function and Diseases.Life (Basel, Switzerland) · 2023
    Review
  9. The role of tensins in malignant neoplasms.Archives of medical science : AMS · 2023
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

7 authors at 2 institutions in 1 country.

Danuta MartuszewskaDepartment of Laboratory Medicine, Section for Clinical Chemistry, Lund University, University Hospital Malmö, Malmö, Sweden.
Börje Ljungberg
Martin Johansson
Göran Landberg
Cecilia Oslakovic
Björn Dahlbäck
Sassan Hafizi
Lund University · SEUmeå University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe Tensin family of intracellular proteins (Tensin1, -2, -3 and -4) are thought to act as links between the extracellular matrix and the cytoskeleton, and thereby mediate signaling for cell shape and motility. Dysregulation of Tensin expression has previously been implicated in human cancer. Here, we have for the first time evaluated the significance of all four Tensins in a study of human renal cell carcinoma (RCC), as well as probed the biological function of Tensin3. PRINCIPAL

findingsExpression of Tensin2 and Tensin3 at mRNA and protein levels was largely absent in a panel of diverse human cancer cell lines. Quantitative RT-PCR analysis revealed mRNA expression of all four Tensin genes to be significantly downregulated in human kidney tumors (50-100% reduction versus normal kidney cortex; P<0.001). Furthermore, the mRNA expressions of Tensins mostly correlated positively with each other and negatively with tumor grade, but not tumor size. Immunohistochemical analysis revealed Tensin3 to be present in the cytoplasm of tubular epithelium in normal human kidney sections, whilst expression was weaker or absent in 41% of kidney tumors. A subset of tumor sections showed a preferential plasma membrane expression of Tensin3, which in clear cell RCC patients was correlated with longer survival. Stable expression of Tensin3 in HEK 293 cells markedly inhibited both cell migration and matrix invasion, a function independent of putative phosphatase activity in Tensin3. Conversely, siRNA knockdown of endogenous Tensin3 in human cancer cells significantly increased their migration.

conclusionsOur findings indicate that the Tensins may represent a novel group of metastasis suppressors in the kidney, the loss of which leads to greater tumor cell motility and consequent metastasis. Moreover, tumorigenesis in the human kidney may be facilitated by a general downregulation of Tensins. Therefore, anti-metastatic therapies may benefit from restoring or preserving Tensin expression in primary tumors.

Indexed as

Cell MovementAdultAgedAged, 80 and overCarcinoma, Renal CellCell Line, TumorCell ProliferationDown-RegulationFemaleGene Expression Regulation, NeoplasticGene SilencingHumansImmunohistochemistryKidneyKidney NeoplasmsMaleMicrofilament ProteinsRNA, MessengerRNA, Small InterferingTensinsTNS1 protein, humanTNS3 protein, human

Identifiers

PMID19194507
PMCPMC2632886
OpenAlexW1988849263

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.