Evidence map›Paper›PMID 34716430›Full record

ArticleOncogene2022

CMAHP promotes metastasis by reducing ubiquitination of Snail and inducing angiogenesis via GM-CSF overexpression in gastric cancer.

Hsiang-Wei Huang, Ching-Ying Chen, Ya-Hui Huang, Chau-Ting Yeh, Chia-Siu Wang, Cheng-Chih Chang, Kwang-Huei Lin

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

15 citing papers in PubMed, 15 citations in OpenAlex.

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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 4 institutions in 1 country.

Hsiang-Wei HuangDepartment of Biochemistry, College of Medicine, Chang Gung University, Taoyuan, Taiwan.ORCID http://orcid.org/0000-0001-5590-7695
Ching-Ying ChenDepartment of Biochemistry, College of Medicine, Chang Gung University, Taoyuan, Taiwan.
Ya-Hui HuangLiver Research Center, Chang Gung Memorial Hospital, Linkou, Taoyuan, Taiwan.
Chau-Ting YehLiver Research Center, Chang Gung Memorial Hospital, Linkou, Taoyuan, Taiwan.
Chia-Siu WangDepartment of General Surgery, Chang Gung Memorial Hospital at Chia-yi, Chia-yi, Taiwan.ORCID http://orcid.org/0000-0002-9357-2571
Cheng-Chih ChangDepartment of General Surgery, Chang Gung Memorial Hospital at Chia-yi, Chia-yi, Taiwan.
Kwang-Huei LinDepartment of Biochemistry, College of Medicine, Chang Gung University, Taoyuan, Taiwan. khlin@mail.cgu.edu.tw.ORCID http://orcid.org/0000-0002-5649-2222
Chang Gung Memorial Hospital · TWChang Gung University · TWChiayi Chang Gung Memorial Hospital · TWChang Gung University of Science and Technology · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pseudogenes are generally considered "junk" DNA or "genomic fossils" generated during the evolution process that lack biological activity. However, accumulating reports indicate that pseudogenes have biological functions critical for cancer development. Experiments from the current study showed marked overexpression of the cytidine monophospho-N-acetylneuraminic acid hydroxylase pseudogene (CMAHP) in gastric cancer, which was associated with poor overall survival. However, the mechanisms underlying the activity of CMAHP in tumor development are largely unknown. Gene Set Enrichment Analysis (GSEA) revealed that CMAHP-correlated genes are significantly involved in epithelial-mesenchymal transition (EMT) and angiogenesis. Functional studies further confirmed that CMAHP mediates metastasis and angiogenesis in vitro and in vivo. Furthermore, CMAHP promoted cancer cell migration, invasion, and metastasis through Snail overexpression, which decreased ubiquitination mediated by NF-κB signaling. Angiogenesis is known to be induced by granulocyte-macrophage colony-stimulating factor (GM-CSF) stimulation. CMAHP increased GM-CSF transactivation via promoting direct binding of c-Jun to the -1981/-1975 region of the GM-CSF promoter. Notably, CMAHP interacts with Histone H1.4 promoting histone acetylation to enhance c-Jun and RelA (p65) expression. Our collective findings provide novel evidence that CMAHP contributes to tumor progression and modulates metastasis and angiogenesis in gastric cancer.

Indexed as

Angiogenesis Inducing AgentsCell Line, TumorGranulocyte-Macrophage Colony-Stimulating FactorHumansStomach NeoplasmsSurvival AnalysisUbiquitinationAngiogenesis Inducing AgentsGranulocyte-Macrophage Colony-Stimulating Factor

Identifiers

PMID34716430
OpenAlexW3210956140

What Socratic holds

Textmetadata
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 Socratic graph.