Evidence map›Paper›PMID 17521951›Full record

ReviewThe international journal of biochemistry & cell biology2008

Deleted in liver cancer-1 (DLC-1): a tumor suppressor not just for liver.

Yi-Chun Liao, Su Hao Lo

Abstract readReview
In one paragraph

Review in The international journal of biochemistry & cell biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

69 citing papers in PubMed, 118 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. The role of tensins in malignant neoplasms.Archives of medical science : AMS · 2023
    Article
  5. Review
  6. Article
  7. Genes & diseases · 2022
    Article
  8. Role of Constitutive STAR in Leydig Cells.International journal of molecular sciences · 2021
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. The tumor suppressor DLC1 inhibits cancer progression and oncogenic autophagy in hepatocellular carcinoma.Laboratory investigation; a journal of technical methods and pathology · 2018
    Article
  20. Article

9 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

2 authors at 1 institution in 1 country.

Yi-Chun LiaoLawrence Ellison Center for Tissue Regeneration and Repair, Department of Biochemistry and Molecular Medicine, University of California, Davis, Sacramento, CA 95817, USA.
Su Hao Lo
University of California, Davis · US

Funding

Role of Cten in Prostate CancerR01CA102537 · NCI · UNIVERSITY OF CALIFORNIA DAVIS · PI LO, SU HAO · 2004 to 2016
$2.4M
Role of Cten in Prostate CancerR56CA102537 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI LO, SU HAO · 2009 to 2009
$240k
NCI NIH HHS CA102537NCI NIH HHS R01 CA102537NCI NIH HHS R56 CA102537
6 · The paper itself

Abstract

Deleted in liver cancer 1 (DLC-1), as its name implied, was originally isolated as a potential tumor suppressor gene often deleted in hepatocellular carcinoma. Further studies have indicated that down-expression of DLC-1 either by genomic deletion or DNA methylation is associated with a variety of cancer types including lung, breast, prostate, kidney, colon, uterus, ovary, and stomach. Re-expression of DLC-1 in cancer cells regulates the structure of actin cytoskeleton and focal adhesions and significantly inhibits cell growth, supporting its role as a tumor suppressor. This tumor suppressive function relies on DLC-1's RhoGTPase activating protein (RhoGAP) activity and steroidogenic acute regulatory (StAR)-related lipid transfer (START) domain, as well as its focal adhesion localization, which is recruited by the Src Homology 2 (SH2) domains of tensins in a phosphotyrosine-independent fashion. Therefore, the expression and subcellular localization of DLC-1 could be a useful molecular marker for cancer prognosis, whereas DLC-1 and its downstream signaling molecules might be therapeutic targets for the treatment of cancer.

Indexed as

AnimalsCarcinoma, HepatocellularGene Expression RegulationGTPase-Activating ProteinsHumansLiver NeoplasmsMiceNeoplasmsProtein Structure, TertiaryRatsTumor Suppressor ProteinsDLC1 protein, humanGTPase-Activating ProteinsTumor Suppressor Proteins

Identifiers

PMID17521951
PMCPMC2323245
OpenAlexW2168717243

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.