Evidence map›Paper›PMID 28131747›Full record

ArticleEBioMedicine2017

MeCP2 Promotes Gastric Cancer Progression Through Regulating FOXF1/Wnt5a/β-Catenin and MYOD1/Caspase-3 Signaling Pathways.

Lingyu Zhao, Yingxun Liu, Dongdong Tong, Yannan Qin, Juan Yang, Meng Xue, Ning Du, Liying Liu, Bo Guo, Ni Hou and 7 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
8.1field-weighted citation impact, top 2% 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

55 citing papers in PubMed, 82 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 2 institutions in 1 country.

Lingyu ZhaoDepartment of Cell Biology and Genetics, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Shaanxi, Xi'an 710061, People's Republic of China; Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education of China, Shaanxi, Xi'an 710061, People's Republic of China.
Yingxun LiuDepartment of Cell Biology and Genetics, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Shaanxi, Xi'an 710061, People's Republic of China.
Dongdong TongDepartment of Cell Biology and Genetics, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Shaanxi, Xi'an 710061, People's Republic of China.
Yannan QinDepartment of Cell Biology and Genetics, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Shaanxi, Xi'an 710061, People's Republic of China.
Juan YangDepartment of Cell Biology and Genetics, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Shaanxi, Xi'an 710061, People's Republic of China; Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education of China, Shaanxi, Xi'an 710061, People's Republic of China.
Meng XueDepartment of Cell Biology and Genetics, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Shaanxi, Xi'an 710061, People's Republic of China.
Ning DuDepartment of Oncology Surgery, the First Affiliated Hospital of Medical College, Xi'an Jiaotong University, Shaanxi, Xi'an 710061, People's Republic of China.
Liying LiuKey Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education of China, Shaanxi, Xi'an 710061, People's Republic of China.
Bo GuoDepartment of Cell Biology and Genetics, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Shaanxi, Xi'an 710061, People's Republic of China.
Ni HouDepartment of Cell Biology and Genetics, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Shaanxi, Xi'an 710061, People's Republic of China.
Jia HanDepartment of Cell Biology and Genetics, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Shaanxi, Xi'an 710061, People's Republic of China.
Siyuan LiuDepartment of Cell Biology and Genetics, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Shaanxi, Xi'an 710061, People's Republic of China.
Na LiuDepartment of Cell Biology and Genetics, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Shaanxi, Xi'an 710061, People's Republic of China.
Xiaoge ZhaoKey Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education of China, Shaanxi, Xi'an 710061, People's Republic of China.
Lumin WangDepartment of Cell Biology and Genetics, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Shaanxi, Xi'an 710061, People's Republic of China.
Yanke ChenDepartment of Cell Biology and Genetics, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Shaanxi, Xi'an 710061, People's Republic of China.
Chen HuangDepartment of Cell Biology and Genetics, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Shaanxi, Xi'an 710061, People's Republic of China; Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education of China, Shaanxi, Xi'an 710061, People's Republic of China. Electronic address: hchen@xjtu.edu.cn.
Xi'an Jiaotong University · CNFirst Affiliated Hospital of Xi'an Jiaotong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Methyl-CpG binding protein 2 (MeCP2) has recently been characterized as an oncogene frequently amplified in several types of cancer. However, its precise role in gastric cancer (GC) and the molecular mechanism of MeCP2 regulation are still largely unknown. Here we report that MeCP2 is highly expressed in primary GC tissues and the expression level is correlated with the clinicopathologic features of GC. In our experiments, knockdown of MeCP2 inhibited tumor growth. Molecular mechanism of MeCP2 regulation was investigated using an integrated approach with combination of microarray analysis and chromatin immunoprecipitation sequencing (ChIP-Seq). The results suggest that MeCP2 binds to the methylated CpG islands of FOXF1 and MYOD1 promoters and inhibits their expression at the transcription level. Furthermore, we show that MeCP2 promotes GC cell proliferation via FOXF1-mediated Wnt5a/β-Catenin signaling pathway and suppresses apoptosis through MYOD1-mediated Caspase-3 signaling pathway. Due to its high expression level in GC and its critical function in driving GC progression, MeCP2 represents a promising therapeutic target for GC treatment.

Indexed as

AnimalsApoptosisbeta CateninBlotting, WesternCaspase 3Cell LineCell Line, TumorCell ProliferationDisease ProgressionForkhead Transcription FactorsGene Expression ProfilingGene Expression Regulation, NeoplasticHumansMaleMethyl-CpG-Binding Protein 2Mice, Inbred BALB Cbeta CateninCaspase 3Forkhead Transcription FactorsFOXF1 protein, humanMECP2 protein, humanMethyl-CpG-Binding Protein 2MyoD1 myogenic differentiation proteinMyoD ProteinWnt-5a ProteinWNT5A protein, humanCaspase-3FOXF1Gastric cancerMeCP2MYOD1Wnt5a

Identifiers

PMID28131747
PMCPMC5474507
OpenAlexW2573397582

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.