Evidence map›Paper›PMID 31130822›Full record

ArticleCancer cell international2019

BMX-ARHGAP fusion protein maintains the tumorigenicity of gastric cancer stem cells by activating the JAK/STAT3 signaling pathway.

Xiao-Feng Xu, Feng Gao, Jian-Jiang Wang, Cong Long, Xing Chen, Lan Tao, Liu Yang, Li Ding, Yong Ji

Abstract read
In one paragraph

Article in Cancer cell international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

  1. Targeting the BMX in cancer: molecular mechanisms and emerging therapeutic strategies.Journal of enzyme inhibition and medicinal chemistry · 2026
    Review
  2. Article
  3. Article
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  6. Article
  7. Article
  8. Article
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  10. Fixing the GAP: The role of RhoGAPs in cancer.European journal of cell biology · 2022
    Review
  11. Review
  12. 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.

Xiao-Feng Xu *Clinical Laboratory, Jingjiang People's Hospital, Jingjiang, 214500 People's Republic of China.
Feng Gao *Department of Surgery, Jingjiang People's Hospital, No. 28, Zhongzhou Road, Jingjiang, 214500 Jiangsu People's Republic of China.
Jian-Jiang WangDepartment of Surgery, Jingjiang People's Hospital, No. 28, Zhongzhou Road, Jingjiang, 214500 Jiangsu People's Republic of China.
Cong LongClinical Laboratory, Jingjiang People's Hospital, Jingjiang, 214500 People's Republic of China.
Xing ChenDepartment of Surgery, Jingjiang People's Hospital, No. 28, Zhongzhou Road, Jingjiang, 214500 Jiangsu People's Republic of China.
Lan TaoCentral Laboratory, Jingjiang People's Hospital, Jingjiang, 214500 People's Republic of China.
Liu YangClinical Laboratory, Jingjiang People's Hospital, Jingjiang, 214500 People's Republic of China.
Li DingClinical Laboratory, Jingjiang People's Hospital, Jingjiang, 214500 People's Republic of China.
Yong JiDepartment of Surgery, Jingjiang People's Hospital, No. 28, Zhongzhou Road, Jingjiang, 214500 Jiangsu People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCancer stem cells (CSCs), drug-resistant cancer cell subsets, are known to be responsible for tumor metastasis and relapse. The JAK/STAT pathway, activated by SH2 domain, is known to regulate the tumor growth in gastric cancer (GC). Now, this study was designed to examine whether BMX-ARHGAP affects the GC stem cell properties and the underlying regulatory network via JAK/STAT axis.

methodsBMX-ARHGAP expression was characterized in GC tissues and cells by RT-qPCR and western blot assay. When BMX-ARHGAP was overexpressed or silenced via plasmids or siRNA transfection, the stem cell properties were assessed by determining stem cell markers CD133, CD44, SOX2 and Nanog, followed by cell sphere and colony formation assays. Subsequently, cell proliferation and invasion were examined by conducting EdU and Transwell assays. The JAK/STAT3 signaling pathway activation was inhibited using AG490. ARHGAP12, BMX exon 10-11, BXM-SH2, JAK2 and STAT3 expression patterns were all determined to examine the regulatory network. The stem cell property in nude mice was also tested.

resultsBMX-ARHGAP was determined to be enriched in the GC. Overexpression of BMX-ARHGAP resulted in increased expression of CD133, CD44, SOX2 and Nanog protein, and accelerated proliferation and invasion of CD133

conclusionsThe aforementioned results demonstrated that the BMX-ARHGAP-dependent SH2 domain-JAK/STAT3 axis mediates the maintenance of GC stem cells, benefiting the development of new potential therapeutic targets for GC.

Indexed as

BMX-ARHGAPCancer stem cellsGastric cancerJAK/STAT3 signaling pathwaySrc homology region 2

Identifiers

PMID31130822
PMCPMC6525346

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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.