Evidence map›Paper›PMID 16909102›Full record

ArticleOncogene2007

Silencing of stathmin induces tumor-suppressor function in breast cancer cell lines harboring mutant p53.

E Alli, J-M Yang, W N Hait

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing 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

49 citing papers in PubMed, 97 citations in OpenAlex.

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  13. Stathmin is overexpressed and regulated by mutant p53 in oral squamous cell carcinoma.Journal of experimental & clinical cancer research : CR · 2017
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  20. Overexpression of stathmin is resistant to paclitaxel treatment in patients with non-small cell lung cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
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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

3 authors at 1 institution in 1 country.

E AlliDepartment of Pharmacology, The Cancer Institute of New Jersey, UMDNJ-Robert Wood Johnson Medical School, New Brunswick, NJ 08901, USA.
J-M Yang
W N Hait
Rutgers Cancer Institute of New Jersey

Funding

TRANSCRIPTIONAL PROFILINGP30CA072720 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI Chang S Chan · 1997 to 2026
$94.5M
MOLECULAR DETERMINANTS OF DRUG SENSITIVITYR01CA078695 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI HAIT, WILLIAM N · 1999 to 2003
$643k
NCI NIH HHS CA 72720NCI NIH HHS CA 78695
6 · The paper itself

Abstract

Cancers harboring dominant-negative p53 mutations are often aggressive and difficult to treat. Direct attempts to restore wild-type p53 function have produced little clinical benefit. We investigated whether targeting a p53-target gene could induce certain tumor-suppressor characteristics. We found that inhibition of stathmin, a microtubule regulator that can be transcriptionally repressed by wild-type p53, restored certain wild-type functions to cancer cells with mutant p53. Silencing of stathmin by small interfering RNA (siRNA) in mutant p53 cell lines lowered expression to that observed following activation of wild-type p53 by DNA damage in wild-type p53 cell lines. siRNA-induced repression of stathmin decreased cell proliferation, viability and clonogenicity in mutant p53 cell lines. Furthermore, knockdown of stathmin partially restored cell-cycle regulation and activation of apoptosis. Therefore, targeting stathmin, a gene product that is overexpressed in the presence of mutant p53, may represent a novel approach to treating cancers with aberrant p53 function.

Indexed as

MutationApoptosisBreast NeoplasmsCell CycleCell Line, TumorCell ProliferationCell SurvivalFemaleGene SilencingGene TargetingGrowth InhibitorsHumansStathminTumor Suppressor Protein p53Growth InhibitorsStathminTumor Suppressor Protein p53

Identifiers

PMID16909102
OpenAlexW2087842578

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.