Evidence map›Paper›PMID 24694902›Full record

ArticleThe Journal of investigative dermatology2014

Regulation of fibulin-2 gene expression by integrin α3β1 contributes to the invasive phenotype of transformed keratinocytes.

Dara S Missan, Sridar V Chittur, C Michael DiPersio

Open access · greenAbstract read
In one paragraph

Article in The Journal of investigative dermatology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

19 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Review
  3. The epidermal integrin-mediated secretome regulates the skin microenvironment during tumorigenesis and repair.Matrix biology : journal of the International Society for Matrix Biology · 2024
    Review
  4. Review
  5. Article
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  7. Article
  8. Review
  9. Article
  10. Article
  11. Roles of Fibulin-2 in Carcinogenesis.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
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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

3 authors at 2 institutions in 1 country.

Dara S MissanCenter for Cell Biology and Cancer Research, Albany Medical College, Albany, New York, USA.
Sridar V ChitturCenter for Functional Genomics, University at Albany, Rensselaer, New York, USA.
C Michael DiPersioCenter for Cell Biology and Cancer Research, Albany Medical College, Albany, New York, USA. Electronic address: dipersm@mail.amc.edu.
Albany Medical Center Hospital · USUniversity at Albany, State University of New York · US

Funding

Keratinocyte Integrin Crosstalk During Wound Healing.R01AR063778 · NIAMS · ALBANY MEDICAL COLLEGE · PI DIPERSIO, C. MICHAEL, LAMAR, JOHN · 2013 to 2023
$4.0M
Regulation of MMP-9 mRNA stability and tumor growth by alpha3 beta1 integrinR01CA129637 · NCI · ALBANY MEDICAL COLLEGE · PI DIPERSIO, C. MICHAEL · 2008 to 2020
$3.3M
Age-associated changes in integrin function during cutaneous wound healingR21AR056390 · NIAMS · ALBANY MEDICAL COLLEGE · PI DIPERSIO, C. MICHAEL · 2009 to 2010
$386k
NCI NIH HHS R01 CA129637NCI NIH HHS R01CA129637NIAMS NIH HHS R01 AR063778NIAMS NIH HHS R21 AR056390NIAMS NIH HHS R21AR056390
6 · The paper itself

Abstract

The laminin-binding integrin α3β1 is highly expressed in epidermal keratinocytes, where it regulates both cell-autonomous and paracrine functions that promote wound healing and skin tumorigenesis. However, the roles for α3β1 in regulating gene expression programs that control the behaviors of immortalized or transformed keratinocytes remain underexplored. In the current study, we used a microarray approach to identify genes that are regulated by α3β1 in immortalized keratinocytes. α3β1-Responsive genes included several genes that are involved in extracellular matrix proteolysis or remodeling, including fibulin-2 and secreted protein acidic and rich in cysteine. However, α3β1-dependent induction of specific target genes was influenced by the genetic lesion that triggered immortalization, as α3β1-dependent fibulin-2 expression occurred in cells immortalized by either SV40 large T antigen or p53-null mutation, whereas α3β1-dependent expression of secreted protein acidic and rich in cysteine occurred only in the former cells. Interestingly, quantitative PCR arrays did not reveal strong patterns of α3β1-dependent gene expression in freshly isolated primary keratinocytes, suggesting that this regulation is acquired during immortalization. p53-null keratinocytes transformed with oncogenic RasV12 retained α3β1-dependent fibulin-2 expression, and RNAi-mediated knockdown of fibulin-2 in these cells reduced invasion, although not their tumorigenic potential. These findings demonstrate a prominent role for α3β1 in immortalized/transformed keratinocytes in regulating fibulin-2 and other genes that promote matrix remodeling and invasion.

Indexed as

AnimalsCalcium-Binding ProteinsCarcinoma, Squamous CellCell Line, TransformedCell Transformation, NeoplasticExtracellular Matrix ProteinsGene ExpressionIntegrin alpha3beta1KeratinocytesMice, KnockoutOligonucleotide Array Sequence AnalysisPhenotypeSkin NeoplasmsTumor MicroenvironmentCalcium-Binding ProteinsExtracellular Matrix Proteinsfibulin 2Integrin alpha3beta1

Identifiers

PMID24694902
PMCPMC4134363
OpenAlexW1972995256

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.