Evidence map›Paper›PMID 19442116›Full record

ReviewCurrent drug targets2009

ING proteins as potential anticancer drug targets.

M Unoki, K Kumamoto, C C Harris

Open access · greenAbstract readReview
In one paragraph

Review in Current drug targets, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

14 citing papers in PubMed, 26 citations in OpenAlex.

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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 2 countries.

M UnokiLaboratory for Biomarker, The Institute of Physical and Chemical Research, RIKEN, Tokyo 108-8639, Japan.
K Kumamoto
C C Harris
National Institutes of Health · US

Funding

Inhibitor of Normal Growth (ING)ZIABC010875 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HARRIS, CURTIS · 2009 to 2011
$2.1M
Inhibitor of Normal Growth (ING)Z01BC010875 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HARRIS, CURTIS · 2008 to 2008
$649k
Intramural NIH HHS Z01 BC010875Intramural NIH HHS ZIA BC010875
6 · The paper itself

Abstract

Recent emerging evidence suggests that ING family proteins play roles in carcinogenesis both as oncogenes and tumor suppressor genes depending on the family members and on cell status. Previous results from non-physiologic overexpression experiments showed that all five family members induce apoptosis or cell cycle arrest, thus it had been thought until very recently that all of the family members function as tumor suppressor genes. Therefore restoration of ING family proteins in cancer cells has been proposed as a treatment for cancers. However, ING2 knockdown experiments showed unexpected results: ING2 knockdown led to senescence in normal human fibroblast cells and suppressed cancer cell growth. ING2 is also overexpressed in colorectal cancer, and promotes cancer cell invasion through an MMP13 dependent pathway. Additionally, it was reported that ING2 has two isoforms, ING2a and ING2b. Although expression of ING2a predominates compared with ING2b, both isoforms confer resistance against cell cycle arrest or apoptosis to cancer cells, thus knockdown of both isoforms is critical to remove this resistance. Taken together, these results suggest that ING2 can function as an oncogene in some specific types of cancer cells, indicating restoration of this gene in cancer cells could cause cancer progression. Because knockdown of ING2 suppresses cancer cell invasion and induces apoptosis or cell cycle arrest, ING2 may be an anticancer drug target. In this brief review, we discuss possible clinical applications of ING2 with the latest knowledge of molecular targeted therapies.

Indexed as

Drug Delivery SystemsAnimalsAntineoplastic AgentsApoptosisCancer VaccinesCell CycleGene Expression RegulationHumansNeoplasmsProtein IsoformsTumor Suppressor ProteinsAntineoplastic AgentsCancer VaccinesProtein IsoformsTumor Suppressor Proteins

Identifiers

PMID19442116
PMCPMC2802283
OpenAlexW2000255462

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.