Evidence map›Paper›PMID 21045156›Full record

ArticleCancer research2010

Upregulation of DLX5 promotes ovarian cancer cell proliferation by enhancing IRS-2-AKT signaling.

Yinfei Tan, Mitchell Cheung, Jianming Pei, Craig W Menges, Andrew K Godwin, Joseph R Testa

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 19% 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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Apigenin 7-glucoside reprograms tumor metabolism and enhances immunotherapy efficacy in colorectal cancer via DLX5.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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  16. Cancers · 2021
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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

6 authors at 1 institution in 1 country.

Yinfei TanCancer Biology Program, Fox Chase Cancer Center, Philadelphia, Pennsylvania 19111, USA.
Mitchell Cheung
Jianming Pei
Craig W Menges
Andrew K Godwin
Joseph R Testa
Fox Chase Cancer Center · US

Funding

WORD PROCESSING CENTER--COREP30CA006927 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI Dietmar J Kappes · 1985 to 2026
$138.8M
Therapeutic Micro RNA Strategies for Ovarian CancerP50CA083638 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI DALY, MARY BERYL, REBBECK, TIMOTHY R · 1999 to 2013
$33.6M
Basis for Lymphomagenesis in Akt2 Transgenic MiceR01CA077429 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI TESTA, JOSEPH R. · 1998 to 2013
$4.7M
Exploiting Biological Networks to Improve Clinical Treatment of Ovarian CancerR01CA140323 · NCI · UNIVERSITY OF KANSAS MEDICAL CENTER · PI GODWIN, ANDREW K. · 2010 to 2014
$2.1M
NCI NIH HHS CA06927NCI NIH HHS CA77429NCI NIH HHS P30 CA006927NCI NIH HHS P50 CA083638NCI NIH HHS R01 CA077429NCI NIH HHS R01 CA140323
6 · The paper itself

Abstract

The distal-less homeobox gene (dlx) 5 encodes a transcription factor that controls jaw formation and appendage differentiation during embryonic development. We had previously found that Dlx5 is overexpressed in an Akt2 transgenic model of T-cell lymphoma. To investigate if DLX5 is involved in human cancer, we screened its expression in the NCI 60 cancer cell line panel. DLX5 was frequently upregulated in cell lines derived from several tumor types, including ovarian cancer. We next validated its upregulation in primary ovarian cancer specimens. Stable knockdown of DLX5 by lentivirus-mediated transduction of short hairpin RNA (shRNA) resulted in reduced proliferation of ovarian cancer cells due to inhibition of cell cycle progression in connection with the downregulation of cyclins A, B1, D1, D2, and E, and decreased phosphorylation of AKT. Cell proliferation resumed following introduction of a DLX5 cDNA harboring wobbled mutations at the shRNA-targeting sites. Cell proliferation was also rescued by transduction of a constitutively active form of AKT. Intriguingly, downregulation of IRS-2 and MET contributed to the suppression of AKT signaling. Moreover, DLX5 was found to directly bind to the IRS-2 promoter and augmented its transcription. Knockdown of DLX5 in xenografts of human ovarian cancer cells resulted in markedly diminished tumor size. In addition, DLX5 was found to cooperate with HRAS in the transformation of human ovarian surface epithelial cells. Together, these data suggest that DLX5 plays a significant role in the pathogenesis of some ovarian cancers.

Indexed as

Cell ProliferationSignal TransductionAnimalsBlotting, WesternCell CycleCell Line, TumorCells, CulturedCyclinsFemaleGene Expression Regulation, NeoplasticHomeodomain ProteinsHumansInsulin Receptor Substrate ProteinsMiceMice, SCIDOvarian NeoplasmsCyclinsDLX5 protein, humanHomeodomain ProteinsInsulin Receptor Substrate ProteinsIRS2 protein, humanProto-Oncogene Proteins c-aktTranscription Factors

Identifiers

PMID21045156
PMCPMC3018149
OpenAlexW2095416597

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.