Evidence map›Paper›PMID 10944199›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2000

Contact with fibrillar collagen inhibits melanoma cell proliferation by up-regulating p27KIP1.

P Henriet, Z D Zhong, P C Brooks, K I Weinberg, Y A DeClerck

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

65 citing papers in PubMed, 154 citations in OpenAlex.

  1. The Duality of Collagens in Metastases of Solid Tumors.International journal of molecular sciences · 2025
    Review
  2. Article
  3. Dormancy of cutaneous melanoma.Cancer cell international · 2024
    Review
  4. Review
  5. Article
  6. Microenvironment-mediated cancer dormancy: Insights from metastability theory.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Extracellular Matrix Alterations in Metastatic Processes.International journal of molecular sciences · 2019
    Review
  17. Article
  18. Article
  19. Article
  20. Article

5 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

5 authors at 2 institutions in 1 country.

P HenrietDivision of Hematology-Oncology, Department of Pediatrics, Childrens Hospital Los Angeles, California 90027, USA.
Z D Zhong
P C Brooks
K I Weinberg
Y A DeClerck
Palmetto Hematology Oncology · USUniversity of Southern California · US

Funding

METALLOPROTEINASE INHIBITORS IN TUMOR PROGRESSIONR01CA042919 · NCI · CHILDREN'S HOSPITAL OF LOS ANGELES · PI DECLERCK, YVES A · 1987 to 2008
$2.3M
NCI NIH HHS R01 CA042919NCI NIH HHS R01 CA42919
6 · The paper itself

Abstract

It is known that the extracellular matrix regulates normal cell proliferation, and it is assumed that anchorage-independent malignant cells escape this regulatory function. Here we demonstrate that human M24met melanoma cells remain responsive to growth regulatory signals that result from contact with type I collagen and that the effect on proliferation depends on the physical structure of the collagen. On polymerized fibrillar collagen, M24met cells are growth arrested at the G(1)/S checkpoint and maintain high levels of p27(KIP1) mRNA and protein. In contrast, on nonfibrillar (denatured) collagen, the cells enter the cell cycle, and p27(KIP1) is down-regulated. These growth regulatory effects involve contact between type I collagen and the collagen-binding integrin alpha(2)beta(1), which appears restricted in the presence of fibrillar collagen. Thus melanoma cells remain sensitive to negative growth regulatory signals originating from fibrillar collagen, and the proteolytic degradation of fibrils is a mechanism allowing tumor cells to escape these restrictive signals.

Indexed as

Cell Cycle ProteinsGene Expression Regulation, NeoplasticTumor Suppressor ProteinsApoptosisCell CycleCell DivisionCollagenCyclin-Dependent Kinase Inhibitor p27Cyclin-Dependent KinasesExtracellular Matrix ProteinsHumansIntegrinsKineticsMelanomaMicrotubule-Associated ProteinsTumor Cells, CulturedCell Cycle ProteinsCollagenCyclin-Dependent Kinase Inhibitor p27Cyclin-Dependent KinasesExtracellular Matrix ProteinsIntegrinsMicrotubule-Associated ProteinsTumor Suppressor Proteins

Identifiers

PMID10944199
PMCPMC27660
OpenAlexW2091716776

What OpenQuestion holds

Textmetadata
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.