Evidence map›Paper›PMID 23479505›Full record

ArticleNeoplasia (New York, N.Y.)2013

HMGA2 inhibits apoptosis through interaction with ATR-CHK1 signaling complex in human cancer cells.

Suchitra Natarajan, Sabine Hombach-Klonisch, Peter Dröge, Thomas Klonisch

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

42 citing papers in PubMed, 61 citations in OpenAlex.

  1. Associations ofJournal of Cancer · 2026
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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

4 authors at 2 institutions in 2 countries.

Suchitra NatarajanDepartment of Human Anatomy and Cell Science, Faculty of Medicine, University of Manitoba, Winnipeg, Canada.
Sabine Hombach-Klonisch
Peter Dröge
Thomas Klonisch
University of Manitoba · CANanyang Technological University · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The non-histone chromatin binding protein high mobility group AT-hook 2 (HMGA2) is expressed in stem cells and many cancer cells, including tumor initiating cells, but not translated in normal human somatic cells. The presence of HMGA2 is correlated with advanced neoplastic disease and poor prognosis for patients. We had previously demonstrated a role of HMGA2 in DNA repair pathways. In the present study, we employed different human tumor cell models with endogenous and exogenous expression of HMGA2 and show that upon DNA damage, the presence of HMGA2 caused an increased and sustained phosphorylation of the ataxia telangiectasia and Rad3-related kinase (ATR) and its downstream target checkpoint kinase 1 (CHK1). The presence of activated pCHK1(Ser296) coincided with prolonged G2/M block and increased tumor cell survival, which was enhanced further in the presence of HMGA2. Our study, thus, identifies a novel relationship between the ATR-CHK1 DNA damage response pathway and HMGA2, which may support the DNA repair function of HMGA2 in cancer cells. Furthermore, our data provide a rationale for the use of inhibitors to ATR or CHK1 and HMGA2 in the treatment of HMGA2-positive human cancer cells.

Indexed as

ApoptosisSignal TransductionAtaxia Telangiectasia Mutated ProteinsCell Cycle CheckpointsCell Cycle ProteinsCell Line, TumorCheckpoint Kinase 1DNA DamageGene ExpressionHMGA2 ProteinHumansHydroxyureaNeoplasmsPhosphorylationProtein BindingProtein KinasesAtaxia Telangiectasia Mutated ProteinsATR protein, humanCell Cycle ProteinsCheckpoint Kinase 1CHEK1 protein, humanHMGA2 ProteinHydroxyureaProtein KinasesProtein Serine-Threonine Kinases

Identifiers

PMID23479505
PMCPMC3593150
OpenAlexW1922961650

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.