Evidence map›Paper›PMID 29602199›Full record

ArticleJournal of cellular and molecular medicine2018

Elevated CRB3 expression suppresses breast cancer stemness by inhibiting β-catenin signalling to restore tamoxifen sensitivity.

Pingping Li, Chen Feng, He Chen, Yina Jiang, Fang Cao, Jie Liu, Peijun Liu

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 28% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
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  7. Article
  8. METTL3 promotes colorectal carcinoma progression by regulating the m6A-CRB3-Hippo axis.Journal of experimental & clinical cancer research : CR · 2022
    Article
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  15. The clinicopathological significance of ZNF10 in invasive ductal carcinoma of the breast.International journal of clinical and experimental pathology · 2018
    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

7 authors at 2 institutions in 1 country.

Pingping LiCenter for Translational Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Chen FengDepartment of Oncology, Shaanxi Provincial Corps Hospital, Xi'an, China.
He ChenCenter for Translational Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Yina JiangDepartment of Pathology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Fang CaoCenter for Translational Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Jie LiuCenter for Translational Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Peijun LiuCenter for Translational Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.ORCID 0000-0003-0529-387X
First Affiliated Hospital of Xi'an Jiaotong University · CNShanxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tamoxifen is a first-line drug for hormone therapy (HT) in oestrogen receptor-positive breast cancer patients. However, 20% to 30% of those patients are resistant to tamoxifen treatment. Cancer stem cells (CSCs) have been implicated as one of the mechanisms responsible for tamoxifen resistance. Our previous study indicated that decreased expression of the CRB3 gene confers stem cell characteristics to breast cancer cells. In the current investigation, we found that most of the breast cancer patient tissues resistant to tamoxifen were negative for CRB3 protein and positive for β-catenin protein, in contrast to their matched primary tumours by immunohistochemical analysis. Furthermore, expression of CRB3 mRNA and protein was low, while expression of β-catenin mRNA and protein was high in tamoxifen resistance cells (LCC2 and T47D TamR) contrast to their corresponding cell lines MCF7 and T47D. Similarly, CRB3 overexpression markedly restored the tamoxifen sensitivity of TamR cells by the MTT viability assay. Finally, we found that CRB3 suppressed the stemness of TamR cells by inhibiting β-catenin signalling, which may in turn lead to a decrease in the breast cancer cell population. Furthermore, these findings indicate that CRB3 is an important regulator for breast cancer stemness, which is associated with tamoxifen resistance.

Indexed as

AnimalsAntineoplastic Agents, Hormonalbeta CateninBreast NeoplasmsCell Line, TumorCell ProliferationDrug Resistance, NeoplasmFemaleHumansMembrane GlycoproteinsMice, SCIDNeoplastic Stem CellsTamoxifenWnt Signaling PathwayXenograft Model Antitumor AssaysAntineoplastic Agents, Hormonalbeta CateninCRB3 protein, humanCTNNB1 protein, humanMembrane GlycoproteinsTamoxifenbreast cancercancer stem cellsCRB3tamoxifenβ-catenin

Identifiers

PMID29602199
PMCPMC6010813
OpenAlexW2795197334

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.