Evidence map›Paper›PMID 37446127›Full record

ArticleInternational journal of molecular sciences2023

Identification of Moesin (MSN) as a Potential Therapeutic Target for Colorectal Cancer via the β-Catenin-RUNX2 Axis.

Chien-Yu Huang, Po-Li Wei, Uyanga Batzorig, Precious Takondwa Makondi, Cheng-Chin Lee, Yu-Jia Chang

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

10 citing papers in PubMed, 11 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

6 authors at 5 institutions in 3 countries.

Chien-Yu HuangSchool of Medicine, National Tsing Hua University, Hsinchu 30013, Taiwan.
Po-Li WeiDepartment of Surgery, School of Medicine, College of Medicine, Taipei Medical University, Taipei 11031, Taiwan.ORCID 0000-0002-7275-2661
Uyanga BatzorigDepartment of Dermatology, University of California, San Diego, CA 92093, USA.ORCID 0000-0001-8565-4713
Precious Takondwa MakondiKamuzu Central Hospital, National Cancer Center, Lilongwe P.O. Box 149, Malawi.
Cheng-Chin LeeGraduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei 11031, Taiwan.
Yu-Jia ChangDepartment of Pathology, Wan Fang Hospital, Taipei Medical University, Taipei 11696, Taiwan.ORCID 0000-0003-3978-3244
Taipei Medical University Hospital · TWKamuzu Central Hospital · MWNational Tsing Hua University · TWTaipei Medical University · TWUniversity of California San Diego · US

Funding

Taipei Medical University and Taipei Medical University Hospital (109TMU-TMUH-12).
6 · The paper itself

Abstract

CRC is the second leading cause of cancer-related death. The complex mechanisms of metastatic CRC limit available therapeutic choice. Thus, identifying new CRC therapeutic targets is essential. Moesin (MSN), a member of the ezrin-radixin-moesin family, connects the cell membrane to the actin-based cytoskeleton and regulates cell morphology. We investigated the role of MSN in the progression of CRC. GENT2 and oncomine were used to study MSN expression and CRC patient outcomes. MSN-specific shRNAs or MSN-overexpressed plasmid were used to establish MSN-KD and MSN overexpressed cell lines, respectively. SRB, migration, wound healing, and flow cytometry were used to test cell survival and migration. Propidium iodide and annexin V stain were used to analyze the cell cycle and apoptosis. MSN expression was found to be higher in CRC tissues than in normal tissues. Higher MSN expression is associated with poor overall survival, disease-free survival, and relapse-free survival rates in CRC patients. MSN silencing inhibits cell proliferation, adhesion, migration, and invasion in vitro, whereas MSN overexpression accelerates cell proliferation, adhesion, migration, and invasion. RNA sequencing was used to investigate differentially expressed genes, and RUNX2 was discovered as a possible downstream target for MSN. In CRC patients, RUNX2 expression was significantly correlated with MSN expression. We also found that MSN silencing decreased cytoplasmic and nuclear β-catenin levels. Additionally, pharmacological inhibition of β-catenin in MSN-overexpressed cells led to a reduction of RUNX2, and activating β-catenin signaling by inhibiting GSK3β rescued the RUNX2 downregulation in MSN-KD cells. This confirms that MSN regulates RUNX2 expression via activation of β-catenin signaling. Finally, our result further determined that RUNX2 silencing reduced the ability of MSN overexpression cells to proliferate and migrate. MSN accelerated CRC progression via the β-catenin-RUNX2 axis. As a result, MSN holds the potential to become a new target for CRC treatment.

Indexed as

beta CateninColorectal NeoplasmsCell Line, TumorCell MovementCell ProliferationCore Binding Factor Alpha 1 SubunitGene Expression Regulation, NeoplasticHumansMicrofilament ProteinsWnt Signaling Pathwaybeta CateninCore Binding Factor Alpha 1 SubunitMicrofilament ProteinsmoesinRUNX2 protein, humancolorectal cancerGSK3βinvasionmigrationmoesinproliferationRUNX2β-catenin

Identifiers

PMID37446127
PMCPMC10341927
OpenAlexW4382751876

What OpenQuestion holds

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Registered trials

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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.