Evidence map›Paper›PMID 23135750›Full record

ArticleDigestive diseases and sciences2013

HMGA2 elicits EMT by activating the Wnt/β-catenin pathway in gastric cancer.

Lang Zha, Jing Zhang, Weixue Tang, Neng Zhang, Miao He, Yi Guo, Ziwei Wang

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Article in Digestive diseases and sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

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0cells of the map it votes in
60citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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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.

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3 · Its place in the literature

Who cites it

60 citing papers in PubMed.

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  10. LINC00922 acts as a novel oncogene in gastric cancer.World journal of surgical oncology · 2022
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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Lang ZhaDepartment of Gastrointestinal Surgery, First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, People's Republic of China.
Jing Zhang
Weixue Tang
Neng Zhang
Miao He
Yi Guo
Ziwei Wang

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe high mobility group protein A2 (HMGA2) is an architectural transcription factor that plays an important role in the development and progression of many malignant neoplasms. High expression of HMGA2 in gastric cancer correlates with invasiveness of cancer and is an independent prognostic factor. The reason for this might be HMGA2 promoting epithelial-mesenchymal transitions (EMT), which is the key process of metastasis for some underlying mechanisms.

aimsThis study was designed to test whether HMGA2 participates in the EMT and to further understand the underlying mechanisms of EMT promoted by HMGA2.

methodsWe examined the cell biology and molecular biology changes after overexpression and knockdown HMGA2 of gastric cancer cells in vitro and vivo. To further understand the underlying mechanisms of EMT promoted by HMGA2, based on our previous study, we examined the changes of target genes of HMGA2 after overexpression and knockdown HMGA2 of gastric cancer cells.

resultsThe results indicated that overexpressing HMGA2 enabled enhancing the oncogenic properties of gastric epithelial origin cell in vitro and in vivo. Furthermore, our study showed that HMGA2 was able to elicit EMT and regulate several genes which are closely related to the Wnt/β-catenin pathway by directly binding to their promoter thereby activating the Wnt/β-catenin pathway.

conclusionsThe Wnt/β-catenin pathway activated by HMGA2 might be the underlying mechanism of EMT in gastric cancer cells.

Indexed as

Animalsbeta CateninCell Line, TumorEpithelial CellsEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHMGA2 ProteinHumansMiceMice, Inbred BALB CMice, NudeNeoplasms, ExperimentalNuclear ProteinsRNA, Small InterferingStomachbeta CateninHMGA2 ProteinNuclear ProteinsRNA, Small InterferingTWIST1 protein, humanTwist-Related Protein 1Wnt Proteins

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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.