Evidence map›Paper›PMID 25928539›Full record

ArticlePloS one2015

Elevation of soluble guanylate cyclase suppresses proliferation and survival of human breast cancer cells.

Hui-Chin Wen, Chih-Pin Chuu, Chen-Yu Chen, Shine-Gwo Shiah, Hsing-Jien Kung, Kuang-Liang King, Liang-Chen Su, Shi-Chuan Chang, Chung-Ho Chang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

20 citing papers in PubMed, 46 citations in OpenAlex.

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  7. Unraveling unique and common cell type-specific mechanisms in glioblastoma multiforme.Computational and structural biotechnology journal · 2022
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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

9 authors at 3 institutions in 1 country.

Hui-Chin WenInstitute of Cellular and System Medicine, National Health Research Institutes, Miaoli County, Taiwan.
Chih-Pin ChuuInstitute of Cellular and System Medicine, National Health Research Institutes, Miaoli County, Taiwan.
Chen-Yu ChenInstitute of Cellular and System Medicine, National Health Research Institutes, Miaoli County, Taiwan.
Shine-Gwo ShiahNational Institute of Cancer Research, National Health Research Institutes, Miaoli County, Taiwan.
Hsing-Jien KungInstitute of Molecular and Genomic Medicine, National Health Research Institutes, Miaoli County, Taiwan.
Kuang-Liang KingDivision of General Surgery, Department of Surgery, Taipei Veterans General Hospital, Taipei City, Taiwan.
Liang-Chen SuInstitute of Cellular and System Medicine, National Health Research Institutes, Miaoli County, Taiwan.
Shi-Chuan ChangChest Department, Taipei Veterans General Hospital, Taipei City, Taiwan; Institute of Emergency and Critical Care Medicine, National Yang-Ming University, Taipei City, Taiwan.
Chung-Ho ChangInstitute of Cellular and System Medicine, National Health Research Institutes, Miaoli County, Taiwan; Graduate Institute of Basic Medical Science, Ph.D. Program of Aging, China Medical University, Taichung City, Taiwan.
National Health Research Institutes · TWNational Yang Ming University Hospital · TWTaipei Veterans General Hospital · TW

Funding

Staff InvestigatorsP30CA093373 · NCI · UNIVERSITY OF CALIFORNIA DAVIS · PI Laura Marcu · 2002 to 2026
$84.9M
NCI NIH HHS P30 CA093373
6 · The paper itself

Abstract

Nitric oxide (NO) is an essential signaling molecule in biological systems. Soluble guanylate cyclase (sGC), composing of α1 and β1 subunit, is the receptor for NO. Using radioimmunoassay, we discovered that activation of sGC by treatment with bradykinin or sodium nitroprusside (SNP) is impaired in MCF-7 and MDA-MB-231 breast cancer cells as compared to normal breast epithelial 184A1 cells. The 184A1 cells expressed both sGC α1 and sGCβ1 mRNAs. However, levels of sGCβ1 mRNAs were relatively lower in MCF-7 cells while both mRNA of sGC subunits were absent in MDA-MB-231 cells. Treatment with DNA methyltransferase inhibitor 5-aza-2'-deoxycytidine (5-aza-dC) increased mRNA levels of both sGCα1 and sGCβ1 in MDA-MB-231 cells but only sGCβ1 mRNAs in MCF-7 cells. The 5-aza-dC treatment increased the SNP-induced cGMP production in MCF-7 and MDA-MB-231, but not in 184A1 cells. Bisulfite sequencing revealed that the promoter of sGCα1 in MDA-MB-231 cells and promoter of sGCβ1 in MCF-7 cells were methylated. Promoter hypermethylation of sGCα1 and sGCβ1 was found in 1 out of 10 breast cancer patients. Over-expression of both sGC subunits in MDA-MB-231 cells induced apoptosis and growth inhibition in vitro as well as reduced tumor incidence and tumor growth rate of MDA-MB-231 xenografts in nude mice. Elevation of sGC reduced protein abundance of Bcl-2, Bcl-xL, Cdc2, Cdc25A, Cyclin B1, Cyclin D1, Cdk6, c-Myc, and Skp2 while increased protein expression of p53. Our study demonstrated that down-regulation of sGC, partially due to promoter methylation, provides growth and survival advantage in human breast cancer cells.

Indexed as

AnimalsApoptosisAzacitidineBradykininBreast NeoplasmsCell CycleCell ProliferationCell SurvivalCyclic GMPDecitabineDNA MethylationFemaleGuanylate CyclaseHumansMCF-7 CellsMiceAzacitidineBradykininCyclic GMPDecitabineGuanylate CyclaseNitric OxideNitroprussideReceptors, Cytoplasmic and NuclearSoluble Guanylyl Cyclase

Identifiers

PMID25928539
PMCPMC4416047
OpenAlexW1973596354

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.