Evidence map›Paper›PMID 33108608›Full record

ArticleBreast cancer (Tokyo, Japan)2021

Expression and promoter methylation status of OPCML and its functions in the inhibition of cell proliferation, migration, and invasion in breast cancer.

Bin Lian, Hong Li, Yaobang Liu, Dahai Chai, Yali Gao, Yangyang Zhang, Jia Zhou, Jinping Li

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Article in Breast cancer (Tokyo, Japan), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-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

7 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Downregulation ofFrontiers in oncology · 2025
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  4. Review
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  6. Cancer genomics & proteomics
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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 1 institution in 1 country.

Bin Lian *Department of Oncology Surgery, General Hospital of Ningxia Medical University, Yinchuan, 750004, Ningxia, China.
Hong Li *Department of Oncology Surgery, General Hospital of Ningxia Medical University, Yinchuan, 750004, Ningxia, China.
Yaobang Liu *Department of Oncology Surgery, General Hospital of Ningxia Medical University, Yinchuan, 750004, Ningxia, China.
Dahai ChaiDepartment of Oncology Surgery, General Hospital of Ningxia Medical University, Yinchuan, 750004, Ningxia, China.
Yali GaoNingxia Medical University, Yinchuan, 750004, Ningxia, China.
Yangyang ZhangNingxia Medical University, Yinchuan, 750004, Ningxia, China.
Jia ZhouNingxia Medical University, Yinchuan, 750004, Ningxia, China.
Jinping LiDepartment of Oncology Surgery, General Hospital of Ningxia Medical University, Yinchuan, 750004, Ningxia, China. m16521098620@163.com.
Ningxia Medical University · CN

Funding

National Natural Science Foundation of China (CN) 81760482Natural Science Foundation of Ningxia 2018AAC03162Natural Science Foundation of Ningxia NZ17138
6 · The paper itself

Abstract

backgroundOpioid binding protein/cell adhesion molecule-like (OPCML) has been demonstrated to be a tumor suppressor gene, as it has been shown in previous studies to play a tumor-suppressive role in a variety of cancers. However, the role of OPCML in breast tumorigenesis remains unclear.

methodsIn this study, we analyzed OPCML expression in breast cancers and adjacent non-tumor tissue samples and examined its molecular function in the breast cancer-derived cell lines MDA-MB-231 and MCF7.

resultsWe found that OPCML was downregulated in most breast cancer samples but that this protein was expressed in most adjacent non-tumor samples. The loss or downregulation of OPCML is associated with hypermethylation of its promoter. Methylation of the OPCML promoter was detected in all breast cancer cell lines and primary tumors but was not detected in surgical margin tissues and normal breast tissues. Furthermore, functional assays showed that ectopic OPCML expression could inhibit breast tumor cell proliferation in vivo and in vitro and further suppresses tumor cell migration and invasion.

conclusionOur results show that OPCML exerts its tumor-suppressive functions in human breast cancer cells. Moreover, the promoter-specific hypermethylation of OPCML plays an important role in human breast cancer development.

Indexed as

AdultAgedAnimalsBreast NeoplasmsCell Adhesion MoleculesCell MovementCell ProliferationChinaDNA MethylationDown-RegulationFemaleFollow-Up StudiesGene Expression Regulation, NeoplasticGenes, Tumor SuppressorGPI-Linked ProteinsHumansCell Adhesion MoleculesGPI-Linked ProteinsOPCML protein, humanBreast cancerMethylationMigrationOPCMLProliferation

Identifiers

PMID33108608
OpenAlexW3095332916

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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.