Evidence map›Paper›PMID 23152075›Full record

ArticleOncology reports2013

Early growth response 1 regulates glucose deprivation-induced necrosis.

Hyun Min Jeon, Su Yeon Lee, Min Kyung Ju, Cho Hee Kim, Hye Gyeong Park, Ho Sung Kang

Open access · bronzeAbstract read
In one paragraph

Article in Oncology reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

9 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Regulation of Tumor Progression by Programmed Necrosis.Oxidative medicine and cellular longevity · 2018
    Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. HMGB1 in health and disease.Molecular aspects of medicine · 2014
    Review
  9. Article
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.

Hyun Min JeonDepartment of Molecular Biology, College of Natural Sciences, Pusan National University, Pusan 609-735, Republic of Korea.
Su Yeon Lee
Min Kyung Ju
Cho Hee Kim
Hye Gyeong Park
Ho Sung Kang
Pusan National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Necrosis is commonly found in the core region of solid tumours due to metabolic stress such as hypoxia and glucose deprivation (GD) resulting from insufficient vascularization. Necrosis promotes tumour growth and development by releasing the tumour-promoting cytokine high mobility group box 1 (HMGB1); however, the molecular mechanism underlying necrotic cell death remains largely unknown. In this study, we show that early growth response 1 (Egr-1) is induced in a reactive oxygen species (ROS)-dependent manner by GD in several cell lines such as A549, MDA-MB-231 and HepG2 cells that exhibit necrosis upon GD. We found that Egr-1 short hairpin RNA (shRNA) prevented GD-induced necrosis and HMGB1 release. Necrosis-inhibiting activity of Egr-1 shRNA was also seen in multicellular tumour spheroids (MTSs), an in vitro tumour model system. In contrast, Egr-1 overexpression appeared to make tumour cells more susceptible to GD-induced necrosis. Finally, Egr-1 shRNA suppressed the growth of MTSs. These findings demonstrate that Egr-1 is implicated in GD-induced necrosis and tumour progression.

Indexed as

Early Growth Response Protein 1Gene Expression ProfilingGlucoseHep G2 CellsHMGB1 ProteinHumansMCF-7 CellsNecrosisPlasmidsReactive Oxygen SpeciesRNA, Small InterferingSpheroids, CellularTetradecanoylphorbol AcetateTransfectionEarly Growth Response Protein 1EGR1 protein, humanGlucoseHMGB1 ProteinReactive Oxygen SpeciesRNA, Small InterferingTetradecanoylphorbol Acetate

Identifiers

PMID23152075
PMCPMC3583586
OpenAlexW2067467796

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.