Evidence map›Paper›PMID 26000884›Full record

ArticlePloS one2015

Annexin A1 Preferentially Predicts Poor Prognosis of Basal-Like Breast Cancer Patients by Activating mTOR-S6 Signaling.

Anjana Bhardwaj, Nivetha Ganesan, Kazunoshin Tachibana, Kimal Rajapakshe, Constance T Albarracin, Preethi H Gunaratne, Cristian Coarfa, Isabelle Bedrosian

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 26 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 2 pooled it
2.3field-weighted citation impact, top 12% 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

26 citing papers in PubMed, 2 syntheses or guidelines pooled it, 35 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

8 authors at 3 institutions in 1 country.

Anjana BhardwajDepartment of Surgical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, United States of America.
Nivetha GanesanDepartment of Surgical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, United States of America.
Kazunoshin TachibanaDepartment of Surgical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, United States of America.
Kimal RajapaksheDepartment of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, United States of America.
Constance T AlbarracinDepartment of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, United States of America.
Preethi H GunaratneDepartment of Biology and Biochemistry, University of Houston, Houston, TX, United States of America.
Cristian CoarfaDepartment of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, United States of America.
Isabelle BedrosianDepartment of Surgical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, United States of America.
The University of Texas MD Anderson Cancer Center · USBaylor College of Medicine · USUniversity of Houston · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Fabien Delerue · 1985 to 2026
$290.8M
6 · The paper itself

Abstract

introductionAnnexin A1 (ANXA1) is an anti-inflammatory protein reported to play a role in cell proliferation and apoptosis, and to be deregulated in breast cancer. The exact role of annexin A1 in the biology of breast cancer remains unclear. We hypothesized that the annexin A1 plays an oncogenic role in basal subtype of breast cancer by modulating key growth pathway(s).

methodsBy mining the Cancer Genome Atlas (TCGA)-Breast Cancer dataset and manipulating annexin A1 levels in breast cancer cell lines, we studied the role of annexin A1 in breast cancer and underlying signaling pathways.

resultsOur in-silico analysis of TCGA-breast cancer dataset demonstrated that annexin A1 mRNA expression is higher in basal subtype compared to luminal and HER2 subtypes. Within the basal subtype, patients show significantly poorer overall survival associated with higher expression of annexin A1. In both TCGA patient samples and cell lines, annexin A1 levels were significantly higher in basal-like breast cancer than luminal and Her2/neu-positive breast cancer. Stable annexin A1 knockdown in TNBC cell lines suppressed the mTOR-S6 pathway likely through activation of AMPK but had no impact on the MAPK, c-Met, and EGFR pathways. In a cell migration assay, annexin A1-depleted TNBC cells showed delayed migration as compared to wild-type cells, which could be responsible for poor patient prognosis in basal like breast cancers that are known to express higher annexin A1.

conclusionsOur data suggest that annexin A1 is prognostic only in patients with basal like breast cancer. This appears to be in part due to the role of annexin A1 in activating mTOR-pS6 pathway.

Indexed as

Annexin A1ApoptosisBreast NeoplasmsCell Line, TumorCell ProliferationComputer SimulationErb-b2 Receptor Tyrosine KinasesFemaleGene Expression Regulation, NeoplasticHumansNeoplasms, Basal CellPhosphorylationPrognosisSignal TransductionSurvival RateTOR Serine-Threonine KinasesAnnexin A1Erb-b2 Receptor Tyrosine KinasesTOR Serine-Threonine Kinases

Identifiers

PMID26000884
PMCPMC4441370
OpenAlexW431377614

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.