Evidence map›Paper›PMID 18691013›Full record

ReviewCurrent drug targets2008

Targeting SphK1 as a new strategy against cancer.

Dai Shida, Kazuaki Takabe, Dmitri Kapitonov, Sheldon Milstien, Sarah Spiegel

Open access · greenAbstract readReview
In one paragraph

Review in Current drug targets, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 181 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
181citing papers in PubMed, 2 pooled it
6.9field-weighted citation impact, top 2% 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

181 citing papers in PubMed, 2 syntheses or guidelines pooled it, 306 citations in OpenAlex.

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121 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 1 institution in 1 country.

Dai ShidaDepartment of Biochemistry and Molecular Biology, Virginia Commonwealth University School of Medicine, 1101 E. Marshall Street, 2011 Sanger Hall, Richmond, VA 23298, USA.
Kazuaki Takabe
Dmitri Kapitonov
Sheldon Milstien
Sarah Spiegel
Virginia Commonwealth University · US

Funding

Sphingosine Kinases in Cancer Cell SignalingR01CA061774 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI SPIEGEL, SARAH · 1994 to 2015
$3.8M
Sphingosine-1 phosphate phosphohydrolaseR37GM043880 · NIGMS · VIRGINIA COMMONWEALTH UNIVERSITY · PI SPIEGEL, SARAH · 2003 to 2012
$3.2M
Targeting sphingosine kinases in FceRI-mediated allergic responsesR01AI050094 · NIAID · VIRGINIA COMMONWEALTH UNIVERSITY · PI SPIEGEL, SARAH · 2002 to 2012
$2.9M
TRAINING PROGRAM IN TISSUE REPAIRT32GM008695 · NIGMS · VIRGINIA COMMONWEALTH UNIVERSITY · PI DIEGELMANN, ROBERT F · 1998 to 2009
$958k
Sphingolipid SignalingZIAMH001039 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI MILSTIEN, SHELDON · 2009 to 2009
$83k
Intramural NIH HHSNCI NIH HHS R01 CA061774NCI NIH HHS R01CA61774NIAID NIH HHS R01 AI050094NIAID NIH HHS R01AI50094NIGMS NIH HHS 5T-32GM008695-08NIGMS NIH HHS R37 GM043880NIGMS NIH HHS R37GM043880NIGMS NIH HHS T32 GM008695
6 · The paper itself

Abstract

Sphingolipid metabolites have emerged as critical players in a number of fundamental biological processes. Among them, sphingosine-1-phosphate (S1P) promotes cell survival and proliferation, in contrast to ceramide and sphingosine, which induce cell growth arrest and apoptosis. These sphingolipids with opposing functions are interconvertible inside cells, suggesting that a finely tuned balance between them can determine cell fate. Sphingosine kinases (SphKs), which catalyze the phosphorylation of sphingosine to S1P, are critical regulators of this balance. Of the two identified SphKs, sphingosine kinase type 1 (SphK1) has been shown to regulate various processes important for cancer progression and will be the focus of this review, since much less is known of biological functions of SphK2, especially in cancer. SphK1 is overexpressed in various types of cancers and upregulation of SphK1 has been associated with tumor angiogenesis and resistance to radiation and chemotherapy. Many growth factors, through their tyrosine kinase receptors (RTKs), stimulate SphK1 leading to a rapid increase in S1P. This S1P in turn can activate S1P receptors and their downstream signaling. Conversely, activation of S1P receptors can induce transactivation of various RTKs. Thus, SphK1 may play important roles in S1P receptor RTK amplification loops. Here we review the role of SphK1 in tumorigenesis, hormonal therapy, chemotherapy resistance, and as a prognostic marker. We will also review studies on the effects of SphK inhibitors in cells in vitro and in animals in vivo and in some clinical trials and highlight the potential of SphK1 as a new target for cancer therapeutics.

Indexed as

Drug Delivery SystemsAnimalsAntineoplastic AgentsDrug Resistance, NeoplasmEnzyme InhibitorsGene Expression Regulation, NeoplasticHumansNeoplasmsNeovascularization, PathologicPhosphotransferases (Alcohol Group Acceptor)Sphingosine KinaseAntineoplastic AgentsEnzyme InhibitorsPhosphotransferases (Alcohol Group Acceptor)Sphingosine Kinase

Identifiers

PMID18691013
PMCPMC2674575
OpenAlexW2147245292

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.