Evidence map›Paper›PMID 32741119›Full record

ArticleMolecular oncology2020

Downregulation of STK4 promotes colon cancer invasion/migration through blocking β-catenin degradation.

Cheng-Han Lin, Tai-I Hsu, Pei-Yu Chiou, Michael Hsiao, Wen-Ching Wang, Yu-Chia Chen, Jen-Tai Lin, Jaw-Yuan Wang, Peng-Chan Lin, Forn-Chia Lin and 4 more

Open access · goldAbstract read
In one paragraph

Article in Molecular oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 30% 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

9 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
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  3. Reactivation of the silencedProceedings of the National Academy of Sciences of the United States of America · 2026
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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

14 authors at 8 institutions in 1 country.

Cheng-Han LinInstitute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan.ORCID 0000-0001-5444-3999
Tai-I HsuInstitute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan.ORCID 0000-0002-1904-6290
Pei-Yu ChiouInstitute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Michael HsiaoGenomics Research Center, Academia Sinica, Taipei, Taiwan.ORCID 0000-0001-8529-9213
Wen-Ching WangDepartment of Surgery, Chi Mei Medical Center, Tainan, Taiwan.
Yu-Chia ChenDivision of General Surgery, Department of Surgery, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan.
Jen-Tai LinDivision of Urology, Department of Surgery, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan.
Jaw-Yuan WangInstitute of Clinical Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
Peng-Chan LinDepartment of Internal Medicine, College of Medicine, National Cheng Kung University Hospital, National Cheng Kung University, Tainan, Taiwan.
Forn-Chia LinDepartment of Radiation Oncology, College of Medicine, National Cheng Kung University Hospital, National Cheng Kung University, Tainan, Taiwan.
Yu-Kai TsengDepartment of Orthopedics, Show Chwan Memorial Hospital, Changhua, Taiwan.
Hui-Chuan ChengInstitute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Chi-Long ChenDepartment of Pathology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Pei-Jung LuInstitute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan.ORCID 0000-0002-8143-5668
National Cheng Kung University · TWNational Cheng Kung University Hospital · TWKaohsiung Veterans General Hospital · TWChang Bing Show Chwan Memorial Hospital · TWChi Mei Medical Center · TWGenomics Research Center, Academia Sinica · TWKaohsiung Medical University · TWTaipei Medical University Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mammalian STE20-like kinase 1 (MST1/STK4/KRS2) encodes a serine/threonine kinase that is the mammalian homolog of Drosophila Hippo. STK4 plays an important role in controlling cell growth, apoptosis, and organ size. STK4 has been studied in many cancers with previous studies indicating an involvement in colon cancer lymph node metastasis and highlighting its potential as a diagnostic marker for colon cancer. However, the role of STK4 defect in promoting colon cancer progression is still understudied. Here, we found that STK4 was significantly downregulated in colon cancer and was associated with distal metastasis and poor survival. Furthermore, STK4 knockdown enhanced sphere formation and metastasis in vitro and promoted tumor development in vivo. We found that STK4 colocalized with β-catenin and directly phosphorylated β-catenin resulting in its degradation via the ubiquitin-mediated pathway. This may suggest that STK4 knockdown causes β-catenin phosphorylation failure and subsequently β-catenin accumulation, consequently leading to anchorage-independent growth and metastasis in colon cancer. Our results support that STK4 may act as a potential candidate for the assessment of β-catenin-mediated colon cancer prognosis.

Indexed as

Gene Expression Regulation, NeoplasticProteolysisAgedAnimalsbeta CateninCell Line, TumorCell MovementColonic NeoplasmsDisease ProgressionDown-RegulationFemaleHippo KinasesHumansIntracellular Signaling Peptides and ProteinsMaleMice, Inbred NODbeta CateninHippo KinasesIntracellular Signaling Peptides and ProteinsProtein Serine-Threonine KinasesSTK4 protein, humancolon cancersSTK4β-catenin

Identifiers

PMID32741119
PMCPMC7530774
OpenAlexW3046284137

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.