Evidence map›Paper›PMID 27644439›Full record

ArticleJournal of hematology & oncology2016

Bmi-1 regulates stem cell-like properties of gastric cancer cells via modulating miRNAs.

Xiaofeng Wang, Chang Wang, Xiaowei Zhang, Ruixi Hua, Lu Gan, Mingzhu Huang, Liqin Zhao, Sujie Ni, Weijian Guo

Abstract read
In one paragraph

Article in Journal of hematology & oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
–field-weighted citation impact
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

41 citing papers in PubMed.

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  9. PROX1-mediated epigenetic silencing ofInternational journal of biological sciences · 2023
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  11. Genistein promotes M1 macrophage apoptosis and reduces inflammatory response by disrupting miR-21/TIPE2 pathway.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2022
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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

9 authors.

Xiaofeng WangDepartment of Medical Oncology, Fudan University Shanghai Cancer Center, Shanghai, China.
Chang WangDepartment of Medical Oncology, Fudan University Shanghai Cancer Center, Shanghai, China.
Xiaowei ZhangDepartment of Medical Oncology, Fudan University Shanghai Cancer Center, Shanghai, China.
Ruixi HuaDepartment of Medical Oncology, Fudan University Shanghai Cancer Center, Shanghai, China.
Lu GanDepartment of Medical Oncology, Fudan University Shanghai Cancer Center, Shanghai, China.
Mingzhu HuangDepartment of Medical Oncology, Fudan University Shanghai Cancer Center, Shanghai, China.
Liqin ZhaoDepartment of Medical Oncology, Fudan University Shanghai Cancer Center, Shanghai, China.
Sujie NiDepartment of Medical Oncology, Fudan University Shanghai Cancer Center, Shanghai, China.
Weijian GuoDepartment of Medical Oncology, Fudan University Shanghai Cancer Center, Shanghai, China. guoweijian1@hotmail.com.ORCID 0000-0002-6155-8345

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundB cell-specific Moloney murine leukemia virus integration site 1 (Bmi-1) plays an important role in regulating stemness in some kinds of cancer. However, the mechanisms remain unclear. This study was to investigate whether and how Bmi-1 regulates stemness of gastric cancer.

methodsWe firstly explored the role of Bmi-1 in regulating stem cell-like features in gastric cancer. Secondly, we screened out its downstream miRNAs and clarified whether these miRNAs are involved in the regulation of stemness. Finally, we investigated the mechanisms how Bmi-1 regulates miRNAs.

resultsBmi-1 positively regulates stem cell-like properties of gastric cancer and upregulates miR-21 and miR-34a. There was a positive correlation between Bmi-1 and miR-21 expression in gastric cancer tissues. MiR-21 mediated the function of Bmi-1 in regulating stem cell-like properties, while miR-34a negatively regulates stem cell-like characteristics via downregulating Bmi-1. Bmi-1 binds to PTEN promoter and directly inhibits PTEN and thereafter activates AKT. Bmi-1 also regulates p53 and PTEN via miR-21. Bmi-1 activated NF-kB via AKT and enhanced the binding of NF-kB to the promoter of miR-21 and miR-34a and increased their expression.

conclusionsBmi-1 positively regulates stem cell-like properties via upregulating miR-21, and miR-34a negatively regulates stem cell-like characteristics by negative feedback regulation of Bmi-1 in gastric cancer. Bmi-1 upregulates miR-21 and miR-34a by activating AKT-NF-kB pathway.

Indexed as

Gene Expression Regulation, NeoplasticHumansMicroRNAsNF-kappa BPolycomb Repressive Complex 1Promoter Regions, GeneticProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseSpecimen HandlingStem CellsStomach NeoplasmsTumor Suppressor Protein p53BMI1 protein, humanMicroRNAsMIRN21 microRNA, humanMIRN34 microRNA, humanNF-kappa BPolycomb Repressive Complex 1Proto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanTumor Suppressor Protein p53Bmi-1Cancer stem cellGastric cancermiRNAs

Identifiers

PMID27644439
PMCPMC5029045

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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.