Evidence map›Paper›PMID 10822371›Full record

ArticleOncogene2000

The cytokine hepatocyte growth factor/scatter factor inhibits apoptosis and enhances DNA repair by a common mechanism involving signaling through phosphatidyl inositol 3' kinase.

S Fan, Y X Ma, J A Wang, R Q Yuan, Q Meng, Y Cao, J J Laterra, I D Goldberg, E M Rosen

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

64 citing papers in PubMed, 159 citations in OpenAlex.

  1. Trial
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4 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

9 authors at 4 institutions in 1 country.

S FanDepartment of Radiation Oncology, Long Island Jewish Medical Center, Albert Einstein College of Medicine, New York, NY 11040, USA.
Y X Ma
J A Wang
R Q Yuan
Q Meng
Y Cao
J J Laterra
I D Goldberg
E M Rosen
Long Island Jewish Medical Center · USAlbert Einstein College of Medicine · USKennedy Krieger Institute · USMercy Medical Center · US

Funding

BIOCHEMISTRY OF BRAIN TUMOR MICROVESSEL DEVELOPMENTR01NS032148 · NINDS · HUGO W. MOSER RES INST KENNEDY KRIEGER · PI LATERRA, JOHN J · 1995 to 2007
$3.0M
PROTECTION AGAINST APOPTOSIS BY SCATTER FACTORR01ES009169 · NIEHS · LONG ISLAND JEWISH MEDICAL CENTER · PI ROSEN, ELIOT M · 1998 to 2006
$2.3M
NIEHS NIH HHS R01-ES09169NINDS NIH HHS R01-NS CA32148
6 · The paper itself

Abstract

Scatter factor (SF) [aka. hepatocyte growth factor (HGF)] (designated HGF/SF) is a multifunctional cytokine that stimulates tumor cell invasion and angiogenesis. We recently reported that HGF/SF protects epithelial and carcinoma cells against cytotoxicity from DNA-damaging agents and that HGF/SF-mediated cytoprotection was associated with up-regulation of the anti-apoptotic protein Bcl-XL in cells exposed to adriamycin. We now report that in addition to blocking apoptosis, HGF/SF markedly enhances the repair of DNA strand breaks caused by adriamycin or gamma radiation. Constitutive expression of Bcl-XL in MDA-MB-453 breast cancer cells not only simulated the HGF/SF-mediated chemoradioresistance, but also enhanced the repair of DNA strand breaks. The ability of HGF/SF to induce both chemoresistance and DNA repair was inhibited by wortmannin, suggesting that these activities of HGF/SF are due, in part, to a phosphatidylinositol-3'-kinase (PI3K) dependent signaling pathway. Consistent with this finding, HGF/SF induced the phosphorylation of c-Akt (protein kinase-B), a PI3K substrate implicated in apoptosis inhibition; and an expression vector encoding a dominant negative kinase inactive Akt partially but significantly inhibited HGF/SF-mediated cell protection and DNA repair. These findings suggest that HGF/SF activates a cell survival and DNA repair pathway that involves signaling through PI3K and c-Akt and stabilization of the expression of Bcl-XL; and they implicate Bcl-XL in the DNA repair process.

Indexed as

Protein Serine-Threonine KinasesAntimutagenic AgentsAntineoplastic AgentsApoptosisbcl-X ProteinBRCA1 ProteinBreast NeoplasmsDNA RepairDose-Response Relationship, RadiationDoxorubicinFemaleGamma RaysHepatocyte Growth FactorHumansMaleMutagensAKT1 protein, humanAntimutagenic AgentsAntineoplastic AgentsBCL2L1 protein, humanbcl-X ProteinBRCA1 ProteinDoxorubicinHepatocyte Growth FactorMutagensPhosphatidylinositol 3-KinasesProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2

Identifiers

PMID10822371
OpenAlexW1999466080

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.