Evidence map›Paper›PMID 35844789›Full record

ArticleInternational journal of biological sciences2022

The TTYH3/MK5 Positive Feedback Loop regulates Tumor Progression via GSK3-β/β-catenin signaling in HCC.

Yixiu Wang, Yuwei Xie, Bingzi Dong, Weijie Xue, Shuhai Chen, Shimada Mitsuo, Hao Zou, Yujie Feng, Kai Ma, Qian Dong and 2 more

Open access · goldAbstract read
In one paragraph

Article in International journal of biological sciences, 2022. 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
1.7field-weighted citation impact, top 17% 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

12 citing papers in PubMed, 13 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

12 authors at 3 institutions in 2 countries.

Yixiu WangDepartment of Hepatobiliary and Pancreatic Surgery, The Affiliated Hospital of Qingdao University, No.16 Jiangsu Road, Qingdao 266003, China.
Yuwei XieDepartment of Hepatobiliary and Pancreatic Surgery, The Affiliated Hospital of Qingdao University, No.16 Jiangsu Road, Qingdao 266003, China.
Bingzi DongShandong Key Laboratory of Digital Medicine and Computer Assisted Surgery, The Affiliated Hospital of Qingdao University, No. 16 Jiangsu Road, Qingdao 266003, China.
Weijie XueDepartment of Gastrointestinal Surgery, The Affiliated Hospital of Qingdao University, No.16 Jiangsu Road, Qingdao 266003, China.
Shuhai ChenDepartment of Surgery, Institute of Biomedical Sciences, Tokushima University, Tokushima 770‑8503, Japan.
Shimada MitsuoDepartment of Surgery, Institute of Biomedical Sciences, Tokushima University, Tokushima 770‑8503, Japan.
Hao ZouDepartment of Hepatobiliary and Pancreatic Surgery, The Affiliated Hospital of Qingdao University, No.16 Jiangsu Road, Qingdao 266003, China.
Yujie FengDepartment of Hepatobiliary and Pancreatic Surgery, The Affiliated Hospital of Qingdao University, No.16 Jiangsu Road, Qingdao 266003, China.
Kai MaDepartment of Hepatobiliary and Pancreatic Surgery, The Affiliated Hospital of Qingdao University, No.16 Jiangsu Road, Qingdao 266003, China.
Qian DongShandong Key Laboratory of Digital Medicine and Computer Assisted Surgery, The Affiliated Hospital of Qingdao University, No. 16 Jiangsu Road, Qingdao 266003, China.
Jingyu CaoDepartment of Hepatobiliary and Pancreatic Surgery, The Affiliated Hospital of Qingdao University, No.16 Jiangsu Road, Qingdao 266003, China.
Chengzhan ZhuDepartment of Hepatobiliary and Pancreatic Surgery, The Affiliated Hospital of Qingdao University, No.16 Jiangsu Road, Qingdao 266003, China.
Qingdao University · CNAffiliated Hospital of Qingdao University · CNTokushima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related death worldwide, and identification of novel targets is necessary for its diagnosis and treatment. This study aimed to investigate the biological function and clinical significance of tweety homolog 3 (TTYH3) in HCC. TTYH3 overexpression promoted cell proliferation, migration, and invasion and inhibited HCCM3 and Hep3B cell apoptosis. TTYH3 promoted tumor formation and metastasis

Indexed as

Carcinoma, HepatocellularLiver Neoplasmsbeta CateninCateninsCell Line, TumorCell MovementCell ProliferationChloride ChannelsEpithelial-Mesenchymal TransitionFeedbackGene Expression Regulation, NeoplasticGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansIntracellular Signaling Peptides and ProteinsProtein Serine-Threonine Kinasesbeta CateninCateninsChloride ChannelsGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaIntracellular Signaling Peptides and ProteinsMAP-kinase-activated kinase 5Protein Serine-Threonine KinasesTTYH3 protein, humanepithelial-mesenchymal transitionhepatocellular carcinomapositive feedbacktumor metastasisTweety homolog 3

Identifiers

PMID35844789
PMCPMC9274494
OpenAlexW4285285816

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.