Evidence map›Paper›PMID 26686084›Full record

ArticleOncogene2016

Regulation of breast tumorigenesis through acid sensors.

S C Gupta, R Singh, M Asters, J Liu, X Zhang, M R Pabbidi, K Watabe, Y-Y Mo

Abstract read
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing 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

44 citing papers in PubMed, 82 citations in OpenAlex.

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  19. Expression Profiles of ASIC1/2 and TRPV1/4 in Common Skin Tumors.International journal of molecular sciences · 2021
    Article
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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

8 authors at 3 institutions in 1 country.

S C GuptaCancer Institute, University of Mississippi Medical Center, Jackson, MS, USA.
R SinghCancer Institute, University of Mississippi Medical Center, Jackson, MS, USA.
M AstersCancer Institute, University of Mississippi Medical Center, Jackson, MS, USA.
J LiuCancer Institute, University of Mississippi Medical Center, Jackson, MS, USA.
X ZhangCenter of Biostatistics and Bioinformatics, University of Mississippi Medical Center, Jackson, MS, USA.
M R PabbidiDepartment of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, MS, USA.
K WatabeDepartment of Cancer Biology, Wake Forest University School of Medicine, Winston Salem, NC, USA.
Y-Y MoCancer Institute, University of Mississippi Medical Center, Jackson, MS, USA.
University of Mississippi Medical Center · USJackson Memorial Hospital · USWake Forest University · US

Funding

Center for Psychiatric NeuroscienceP30GM103328 · NIGMS · UNIVERSITY OF MISSISSIPPI MED CTR · PI STOCKMEIER, CRAIG ALLEN · 2013 to 2017
$5.5M
The Akt-associated microRNAs in cancer cellsR01CA154989 · NCI · UNIVERSITY OF MISSISSIPPI MED CTR · PI MO, YIN-YUAN · 2011 to 2015
$1.5M
NCI NIH HHS R01 CA154989NIGMS NIH HHS P30 GM103328
6 · The paper itself

Abstract

The low extracellular pH in the microenvironment has been shown to promote tumor growth and metastasis; however, the underlying mechanism is poorly understood. Particularly, little is known how the tumor cell senses the acidic signal to activate the acidosis-mediated signaling. In this study, we show that breast cancer cells express acid-sensing ion channel 1 (ASIC1), a proton-gated cation channel primarily expressed in the nervous system. RNA interference, knockout and rescue experiments demonstrate a critical role for ASIC1 in acidosis-induced reactive oxidative species and NF-κB activation, two key events for tumorigenesis. Mechanistically, ASIC1 is required for acidosis-mediated signaling through calcium influx. We show that as a cytoplasmic membrane protein, ASIC1 is also associated with mitochondria, suggesting that ASIC1 may regulate mitochondrial calcium influx. Importantly, interrogation of the Cancer Genome Atlas breast invasive carcinoma data set indicates that alterations of ASIC1 alone or combined with other 4 ASIC genes are significantly correlated with poor patient survival. Furthermore, ASIC1 inhibitors cause a significant reduction of tumor growth and tumor load. Together, these results suggest that ASIC1 contributes to breast cancer pathogenesis in response to acidic tumor microenvironments, and ASIC1 may serve as a prognostic marker and a therapeutic target for breast cancer.

Indexed as

AcidosisAcid Sensing Ion ChannelsAnimalsBreast NeoplasmsCalciumCell Line, TumorExtracellular Signal-Regulated MAP KinasesFemaleHumansHydrogen-Ion ConcentrationLung NeoplasmsMiceNeoplasm InvasivenessProto-Oncogene Proteins c-aktReactive Oxygen SpeciesAcid Sensing Ion ChannelsASIC1 protein, humanCalciumExtracellular Signal-Regulated MAP KinasesProto-Oncogene Proteins c-aktReactive Oxygen Species

Identifiers

PMID26686084
PMCPMC6450404
OpenAlexW2339287322

What OpenQuestion holds

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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.