Evidence map›Paper›PMID 32810922›Full record

ArticleFEBS open bio2020

Upregulation of CIP2A in estrogen depletion-resistant breast cancer cells treated with low-dose everolimus.

Eiji Nishio, Takanori Hayashi, Mao Akaza, Yukiko Hisatomi, Masahiro Hikichi, Takuma Fujii, Toshiaki Utsumi, Nobuhiro Harada, Yohei Shimono

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in FEBS open bio, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.4field-weighted citation impact, top 34% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. Article
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 1 institution in 1 country.

Eiji NishioDepartment of Obstetrics and Gynecology, Fujita Health University School of Medicine, Toyoake, Japan.
Takanori HayashiDepartment of Biochemistry, Fujita Health University School of Medicine, Toyoake, Japan.ORCID 0000-0002-2919-9733
Mao AkazaDepartment of Biochemistry, Fujita Health University School of Medicine, Toyoake, Japan.
Yukiko HisatomiDepartment of Biochemistry, Fujita Health University School of Medicine, Toyoake, Japan.
Masahiro HikichiDepartment of Breast Surgery, Fujita Health University School of Medicine, Toyoake, Japan.
Takuma FujiiDepartment of Obstetrics and Gynecology, Fujita Health University School of Medicine, Toyoake, Japan.
Toshiaki UtsumiDepartment of Breast Surgery, Fujita Health University School of Medicine, Toyoake, Japan.
Nobuhiro HaradaDepartment of Biochemistry, Fujita Health University School of Medicine, Toyoake, Japan.
Yohei ShimonoDepartment of Biochemistry, Fujita Health University School of Medicine, Toyoake, Japan.
Fujita Health University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Everolimus (EVE), an inhibitor of mammalian target of rapamycin, is an emerging second-line therapeutic option for hormone therapy-resistant breast cancers. However, some patients do not respond to EVE, whereas in others it exacerbates the disease. Cellular inhibitor of protein phosphatase 2A (CIP2A) is a human oncoprotein that can promote cancer cell growth and apoptosis resistance. Although CIP2A is upregulated in hormone-related cancers, such as breast cancer, little is known about potential anti-tumor effects of downregulating CIP2A. As a model to study the resistance of breast cancer cells to hormone treatment, we previously established clones of long-term estrogen depletion-resistant MCF-7 (LTED) cells. Here, we selected three clones highly responsive to EVE and three clones poorly responsive to EVE. When cells were treated with EVE, CIP2A mRNA expression was decreased in highly responsive EVE clones (DC-cells) whereas it was increased in poorly responsive EVE clones (IC-cells). Using Kaplan-Meier survival plots, we report that high expression of CIP2A was associated with significantly reduced overall survival in patients with luminal A breast cancer. In IC-cells, cell growth was enhanced upon EVE treatment whereas an EVE range of 0.1-100 nm decreased growth in DC-cells. The mRNA expression of genes involved in epithelial-mesenchymal transition (EMT) such as CDH1, CLDN3, and CK19 was significantly decreased in IC-cells, but remained unchanged in DC-cells. These findings highlight a relationship between CIP2A and EMT in the intrinsic resistance of hormone therapy-resistant breast cancers to EVE.

Indexed as

ApoptosisAutoantigensBreast NeoplasmsCell Line, TumorCell ProliferationEpithelial-Mesenchymal TransitionEstrogensEverolimusFemaleGene ExpressionGene Expression ProfilingGene Expression Regulation, NeoplasticHumansIntracellular Signaling Peptides and ProteinsMembrane ProteinsProto-Oncogene Proteins c-aktAutoantigensCIP2A protein, humanEstrogensEverolimusIntracellular Signaling Peptides and ProteinsMembrane ProteinsProto-Oncogene Proteins c-aktAktbreast cancerCIP2Aestrogen receptoreverolimus

Identifiers

PMID32810922
PMCPMC7530388
OpenAlexW3071727727

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.