Evidence map›Paper›PMID 36371204›Full record

ArticleJournal of translational medicine2022

MICAL1 facilitates pancreatic cancer proliferation, migration, and invasion by activating WNT/β-catenin pathway.

Kun Cai, Lu Deng, Dijie Zheng, Lin Li, Zhiwei He, Chao Yu

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 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
1.8field-weighted citation impact, top 14% 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, 21 citations in OpenAlex.

  1. Proteomics in pancreatic cancer.Biomarker research · 2025
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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 3 institutions in 1 country.

Kun Cai *Department of Hepatic-Biliary-Pancreatic Surgery, The Affiliated Hospital of Guizhou Medical University, No.28 Guiyi Street, Yunyan District, Guiyang, 550001, Guizhou, China.
Lu Deng *Guizhou Provincial Staff Hospital, Guiyang, China.
Dijie Zheng *Department of Hepatic-Biliary-Pancreatic Surgery, The Affiliated Hospital of Guizhou Medical University, No.28 Guiyi Street, Yunyan District, Guiyang, 550001, Guizhou, China.
Lin LiDepartment of Hepatic-Biliary-Pancreatic Surgery, The Affiliated Hospital of Guizhou Medical University, No.28 Guiyi Street, Yunyan District, Guiyang, 550001, Guizhou, China.
Zhiwei HeDepartment of Hepatobiliary Surgery, Shenzhen Key Laboratory, Shenzhen University General Hospital, Xueyuan AVE 1098, Nanshan District, Shenzhen, 518055, Guangdong, China. hezhiweigmu@163.com.
Chao YuDepartment of Hepatic-Biliary-Pancreatic Surgery, The Affiliated Hospital of Guizhou Medical University, No.28 Guiyi Street, Yunyan District, Guiyang, 550001, Guizhou, China. yuchao2002@gmc.edu.cn.ORCID 0000-0002-9244-9416
Guiyang Medical University · CNGuizhou Provincial People's Hospital · CNShenzhen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMICAL1 is involved in the malignant processes of several types of cancer; however, the role of MICAL1 in pancreatic cancer (PC) has not been well-characterized. This study aimed to investigate the expression and function of MICAL1 in PC.

methodsRT-qPCR and immunohistochemistry were used to detect MICAL1 expression in PC and adjacent nontumor tissues. Cell Counting Kit-8, EdU, clone formation, wound healing, and Transwell assays as well as animal models were used to investigate the effects of overexpression or inhibition of MICAL1 expression on the proliferation, invasion, and metastasis of PC cells. RNA-seq was used to explore the main pathway underlying the functions of MICAL1. Proteomics, mass spectrometry, and co-immunoprecipitation assays were used to investigate the interaction of proteins with MICAL1. Rescue experiments were conducted to validate these findings.

resultsBoth MICAL1 mRNA and protein levels were upregulated in PC tissues compared with matched adjacent nontumor tissues. The expression level of MICAL1 was associated with the proliferative and metastatic status of PC. Repression of MICAL1 significantly inhibited PC cell growth, migration, and invasion in vitro and in vivo. RNA sequencing analysis indicated that MICAL1 was closely correlated with the WNT pathway. Overexpression of MICAL1 (1) promoted the phosphorylation of TBC1D1 at the Ser660 site, (2) facilitated the distribution of FZD7 on the cytomembrane, (3) inhibited the degradation of FZD7 in the lysosome, and (4) activated the WNT pathway.

conclusionsMICAL1 was upregulated in PC and involved in stimulating the progression of PC cells by activating the WNT/β-catenin signaling pathway. Therefore, MICAL1 is a potential therapeutic target for PC.

Indexed as

Pancreatic NeoplasmsWnt Signaling PathwayAnimalsbeta CateninCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, Neoplasticbeta CateninFZD7MICAL1Pancreatic cancerTBC1D1WNT pathway

Identifiers

PMID36371204
PMCPMC9652939
OpenAlexW4309072439

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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.