Evidence map›Paper›PMID 17078868›Full record

ArticleBreast cancer research : BCR2006

Suppression of breast cancer cell growth by Na+/H+ exchanger regulatory factor 1 (NHERF1).

Yong Pan, Lei Wang, Jia Le Dai

Open access · goldAbstract read
In one paragraph

Article in Breast cancer research : BCR, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 18% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

  1. Pooled it
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  7. NHERF1 and tumor microenvironment: a new scene in invasive breast carcinoma.Journal of experimental & clinical cancer research : CR · 2018
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  9. NHERF1 Enhances Cisplatin Sensitivity in Human Cervical Cancer Cells.International journal of molecular sciences · 2017
    Article
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  11. Deletion of Na+/H+ exchanger regulatory factor 2 represses colon cancer progress by suppression of Stat3 and CD24.American journal of physiology. Gastrointestinal and liver physiology · 2016
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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 1 country.

Yong PanDepartment of Molecular Pathology, The University of Texas M. D. Anderson Cancer Center, Houston, TX 77054, USA. yongpan@mdanderson.org
Lei Wang
Jia Le Dai
The University of Texas MD Anderson Cancer Center · US

Funding

SYK SIGNALING AND BREAST CANCER INVASIONR01CA100278 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI DAI, JIALE · 2003 to 2007
$1.3M
NCI NIH HHS CA100278NCI NIH HHS R01 CA100278
6 · The paper itself

Abstract

introductionNa+/H+ exchanger regulatory factor 1 (NHERF1, also known as EBP50 or NHERF) is a putative tumour suppressor gene in human breast cancer. Located at 17q25.1, NHERF1 is frequently targeted during breast tumourigenesis. Loss of heterozygosity (LOH) at the NHERF1 locus is found in more than 50% of breast tumours. In addition, NHERF1 is mutated in a subset of primary breast tumours and breast cancer cell lines. LOH at the NHERF1 locus is strongly associated with aggressive features of breast tumours, implicating NHERF1 as a haploinsufficiency tumour suppressor gene. However, the putative NHERF1 tumour suppressor activity has not been functionally verified.

methodsTo confirm the NHERF1 tumour suppressor activity suggested by our genetic analyses, we used retrovirus-transduced short hairpin RNA (shRNA) to knock down NHERF1 expression in breast cancer cell lines MCF7 and T47D. These cells were then assessed for cell growth in vitro and in vivo. The control and NHERF1 knockdown cells were also serum-starved and re-fed to compare their cell cycle progression as measured by fluorescence-activated cell sorting analyses.

resultsWe found that downregulation of the endogenous NHERF1 in T47D or MCF7 cells resulted in enhanced cell proliferation in both anchorage-dependent and -independent conditions compared with that of the vector control cells. NHERF1 knockdown T47D cells implanted at mammary fat pads of athymic mice formed larger tumours than did control cells. We found that serum-starved NHERF1 knockdown cells had a faster G1-to-S transition after serum re-stimulation than the control cells. Immunoblotting showed that the accelerated cell cycle progression in NHERF1 knockdown cells was accompanied by increased expression of cyclin E and elevated Rb phosphorylation level.

conclusionOur findings suggested that the normal NHERF1 function in mammary epithelial cells involves blockage of cell cycle progression. Our study affirmed the tumour suppressor activity of NHERF1 in breast which may be related to its regulatory effect on cell cycle. It warrants future investigation of this novel tumour suppressor pathway in human breast cancer which may turn up therapeutic opportunities.

Indexed as

AnimalsBreast NeoplasmsCell CycleCell Line, TumorCell ProliferationEpithelial CellsFemaleGene ExpressionGenes, Tumor SuppressorHumansMicePhosphoproteinsSodium-Hydrogen ExchangersPhosphoproteinssodium-hydrogen exchanger regulatory factorSodium-Hydrogen Exchangers

Identifiers

PMID17078868
PMCPMC1797034
OpenAlexW1717890685

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.