Evidence map›Paper›PMID 15064711›Full record

ArticleOncogene2004

A cytoskeleton-based functional genetic screen identifies Bcl-xL as an enhancer of metastasis, but not primary tumor growth.

Stuart S Martin, Alan G Ridgeway, Jan Pinkas, Yu Lu, Mauricio J Reginato, Eugene Y Koh, Montserrat Michelman, George Q Daley, Joan S Brugge, Philip Leder

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.3field-weighted citation impact, top 14% 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

38 citing papers in PubMed, 75 citations in OpenAlex.

  1. Article
  2. Review
  3. BCL-2 protein family: attractive targets for cancer therapy.Apoptosis : an international journal on programmed cell death · 2023
    Review
  4. Article
  5. Review
  6. iScience · 2021
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. BCL-XCell death & disease · 2017
    Article
  12. Metastasis: an early event in cancer progression.Journal of cancer research and clinical oncology · 2017
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  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

10 authors at 4 institutions in 1 country.

Stuart S MartinHarvard Medical School, Department of Genetics, Howard Hughes Medical Institute, Boston, MA 02115, USA.
Alan G Ridgeway
Jan Pinkas
Yu Lu
Mauricio J Reginato
Eugene Y Koh
Montserrat Michelman
George Q Daley
Joan S Brugge
Philip Leder
Harvard University · USHoward Hughes Medical Institute · USMassachusetts Institute of Technology · USWhitehead Institute for Biomedical Research · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many mouse models of breast cancer form large primary tumors that rarely metastasize. Models with aggressive metastasis express oncoproteins that simultaneously affect growth and apoptosis pathways. To define the role of apoptotic resistance and to model a challenge faced by tumor cells during metastatic dissemination, we focused on apoptosis induced by cell shape change. Inhibiting actin polymerization with Latrunculin-A causes cell rounding and death within hours in nontumorigenic human 10A-Ras mammary epithelial cells. In contrast, MDA-MB-231 metastatic breast tumor cells resist LA-induced death, and survive for days despite cell rounding. Infecting 10A-Ras cells with a MDA-MB-231 retroviral expression library, and selecting with Latrunculin-A repeatedly identified Bcl-xL as a suppressor of cytoskeleton-dependent death. Although Bcl-xL enhances the spread of metastatic breast tumor cell lines, the distinct effects of apoptotic resistance on tumor growth in the mammary gland and during metastasis have not been compared directly. We find that Bcl-xL overexpression in mouse mammary epithelial cells does not induce primary tumor formation or enhance MEK-induced tumorigenesis within the mammary gland environment. However, it strongly enhances metastatic potential. These results with Bcl-xL provide novel evidence that isolated apoptotic resistance can increase metastatic potential, but remain overlooked by assays based on breast tumor growth.

Indexed as

Animalsbcl-X ProteinBreast NeoplasmsBridged Bicyclo Compounds, HeterocyclicCytoskeletonGenetic TechniquesGenetic VectorsHumansMammary Neoplasms, ExperimentalMAP Kinase Kinase 1MiceMitogen-Activated Protein Kinase KinasesNeoplasm MetastasisProto-Oncogene Proteins c-bcl-2ThiazolesThiazolidinesBCL2L1 protein, humanBcl2l1 protein, mousebcl-X ProteinBridged Bicyclo Compounds, Heterocycliclatrunculin AMAP2K1 protein, humanMap2k1 protein, mouseMAP Kinase Kinase 1Mitogen-Activated Protein Kinase KinasesProto-Oncogene Proteins c-bcl-2ThiazolesThiazolidines

Identifiers

PMID15064711
OpenAlexW1996971225

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.