Evidence map›Paper›PMID 25061501›Full record

ArticleGenes & cancer2014

NDRG2 overexpression enhances glucose deprivation-mediated apoptosis in breast cancer cells via inhibition of the LKB1-AMPK pathway.

Hak-Su Kim, Myung-Jin Kim, Jihyun Lim, Young Yang, Myeong-Sok Lee, Jong-Seok Lim

Open access · diamondAbstract read
In one paragraph

Article in Genes & cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

17 citing papers in PubMed, 22 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

6 authors at 1 institution in 1 country.

Hak-Su KimDepartment of Biological Sciences and the Research Center for Women's Diseases, Sookmyung Women's University, Seoul, Republic of Korea.
Myung-Jin KimDepartment of Biological Sciences and the Research Center for Women's Diseases, Sookmyung Women's University, Seoul, Republic of Korea.
Jihyun LimDepartment of Biological Sciences and the Research Center for Women's Diseases, Sookmyung Women's University, Seoul, Republic of Korea.
Young YangDepartment of Biological Sciences and the Research Center for Women's Diseases, Sookmyung Women's University, Seoul, Republic of Korea.
Myeong-Sok LeeDepartment of Biological Sciences and the Research Center for Women's Diseases, Sookmyung Women's University, Seoul, Republic of Korea.
Jong-Seok LimDepartment of Biological Sciences and the Research Center for Women's Diseases, Sookmyung Women's University, Seoul, Republic of Korea.
Sookmyung Women's University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The newly identified tumor suppressor, N-myc downstream-regulated gene 2 (NDRG2), has been studied in various cancers because of its anticancer and antimetastasis effects. In this study, we examined the effect of NDRG2 expression on cell viability in MDA-MB-231 human breast cancer cells under conditions that are similar to the microenvironment of solid tumors, which include glucose deprivation. NDRG2 overexpression enhanced the pro-apoptotic effects of glucose deprivation. Glucose deprivation also induced the activation of AMP-activated protein kinase (AMPK), which plays a role in protecting tumor cells from metabolic stresses. NDRG2 overexpression strongly reduced glucose deprivation-induced AMPK phosphorylation and increased the cleavage of poly (ADP-ribose) polymerase (PARP), which indicated the induction of apoptosis. The expression of a constitutively active form of AMPK effectively blocked glucose deprivation-induced apoptosis in NDRG2-overexpressing MDA-MB-231 cells. Moreover, NDRG2 overexpression also enhanced the pro-apoptotic effects of 2-deoxyglucose (2-DG) or hypoxia, an inducer of metabolic stresses. Finally, we showed that LKB1 is an upstream kinase of AMPK that is involved in the inhibition of glucose deprivation-induced AMPK activity in NDRG2-overexpressing cells. Our findings collectively suggest that NDRG2 is a negative regulator of AMPK activity and functions as a sensitizer of glucose deprivation.

Indexed as

AMPKapoptosisglucose deprivationNDRG2

Identifiers

PMID25061501
PMCPMC4104758
OpenAlexW315031804

What Socratic 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 Socratic graph.