Evidence map›Paper›PMID 35655269›Full record

ArticleJournal of biomedical science2022

DYRK1A reinforces epithelial-mesenchymal transition and metastasis of hepatocellular carcinoma via cooperatively activating STAT3 and SMAD.

Yang-Ling Li, Man-Man Zhang, Lin-Wen Wu, Ye-Han Liu, Zuo-Yan Zhang, Ling-Hui Zeng, Neng-Ming Lin, Chong Zhang

Open access · diamondAbstract read
In one paragraph

Article in Journal of biomedical science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

11 citing papers in PubMed, 19 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

8 authors at 4 institutions in 1 country.

Yang-Ling Li *Department of Clinical Pharmacology, Key Laboratory of Clinical Cancer Pharmacology and Toxicology Research of Zhejiang Province, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, No.261 Huansha Road, Hangzhou, 310006, Zhejiang, China.
Man-Man Zhang *School of Medicine, Zhejiang University City College, No.51 Huzhou Street, Hangzhou, 310015, Zhejiang, China.
Lin-Wen WuSchool of Medicine, Zhejiang University City College, No.51 Huzhou Street, Hangzhou, 310015, Zhejiang, China.
Ye-Han LiuSchool of Medicine, Zhejiang University City College, No.51 Huzhou Street, Hangzhou, 310015, Zhejiang, China.
Zuo-Yan ZhangSchool of Medicine, Zhejiang University City College, No.51 Huzhou Street, Hangzhou, 310015, Zhejiang, China.
Ling-Hui ZengSchool of Medicine, Zhejiang University City College, No.51 Huzhou Street, Hangzhou, 310015, Zhejiang, China. zenglh@zucc.edu.cn.
Neng-Ming LinDepartment of Clinical Pharmacology, Key Laboratory of Clinical Cancer Pharmacology and Toxicology Research of Zhejiang Province, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, No.261 Huansha Road, Hangzhou, 310006, Zhejiang, China. lnm1013@zju.edu.cn.
Chong ZhangSchool of Medicine, Zhejiang University City College, No.51 Huzhou Street, Hangzhou, 310015, Zhejiang, China. zhangchong@zucc.edu.cn.ORCID http://orcid.org/0000-0002-8113-5585
Zhejiang University · CNHangzhou First People's Hospital · CNHuzhou University · CNWestlake University · CN

Funding

National Natural Science Foundation of China 81702887
6 · The paper itself

Abstract

backgroundHepatocellular carcinoma (HCC) accounts for the majority of liver cancer cases, while metastasis is considered the leading cause of HCC-related death. However, the currently available treatment strategies for efficient suppression of metastasis are limited. Therefore, novel therapeutic targets to inhibit metastasis and effectively treat HCC are urgently required.

methodsWound healing and Transwell assays were used to determine the migration and invasion abilities of HCC cells in vitro. Quantitative real-time PCR (qRT-PCR), protein array, immunofluorescence, and immunoprecipitation experiments were used to study the mechanism of DYRK1A-mediated metastasis. A tail vein metastasis model and H&E staining were utilized to assess metastatic potential in vivo.

resultsThe results of the current study demonstrated that dual-specificity tyrosine phosphorylation-regulated kinase 1A (DYRK1A) was upregulated in HCC tissues compared with normal liver tissues. Additionally, the level of DYRK1A was increased in primary HCC tissues of patients with metastasis compared with those of patients without metastasis, and DYRK1A overexpression correlated with worse outcomes in liver cancer patients. Gain- and loss-of-function studies suggested that DYRK1A enhanced the invasion and migration abilities of HCC cells by promoting epithelial-mesenchymal transition (EMT). Regarding the promoting effect of DYRK1A on cell invasion, the results showed that DYRK1A was coexpressed with TGF-β/SMAD and STAT3 signalling components in clinical tumour samples obtained from patients with HCC. DYRK1A also activated TGF-β/SMAD signalling by interacting with tuberous sclerosis 1 (TSC1) and enhanced metastasis of HCC cells by activating STAT3. Furthermore, DYRK1A promoted EMT by cooperatively activating STAT3/SMAD signalling.

conclusionOverall, the present study not only uncovered the promoting effect of DYRK1A on HCC metastasis and revealed the mechanism but also provided a new approach to predict and treat metastatic HCC.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsCell Line, TumorCell MovementEpithelial-Mesenchymal TransitionHumansSTAT3 Transcription FactorTransforming Growth Factor betaSTAT3 protein, humanSTAT3 Transcription FactorTransforming Growth Factor betaDYRK1AEMTHepatocellular carcinomaMetastasisTSC1

Identifiers

PMID35655269
PMCPMC9164892
OpenAlexW4281680388

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.