Evidence map›Paper›PMID 35392973›Full record

ArticleJournal of experimental & clinical cancer research : CR2022

ZMAT1 acts as a tumor suppressor in pancreatic ductal adenocarcinoma by inducing SIRT3/p53 signaling pathway.

Zuyi Ma, Zhenchong Li, Shujie Wang, Zixuan Zhou, Chunsheng Liu, Hongkai Zhuang, Qi Zhou, Shanzhou Huang, Chuanzhao Zhang, Baohua Hou

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

25 citing papers in PubMed, 40 citations in OpenAlex.

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  10. SIRT3/6/7: promising therapeutic targets for pulmonary fibrosis.Frontiers in cell and developmental biology · 2025
    Review
  11. Article
  12. Roles of SIRT3 in aging and aging-related diseases.International journal of biological sciences · 2025
    Review
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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

10 authors at 5 institutions in 1 country.

Zuyi Ma *Department of General Surgery, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, 510080, China.
Zhenchong Li *Department of General Surgery, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, 510080, China.
Shujie Wang *Department of General Surgery, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, 510080, China.
Zixuan ZhouDepartment of General Surgery, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, 510080, China.
Chunsheng LiuDepartment of General Surgery, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, 510080, China.
Hongkai ZhuangDepartment of General Surgery, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, 510080, China.
Qi ZhouDepartment of General Surgery, Hui Ya Hospital of The First Affiliated Hospital, Sun Yat-Sen University, Huizhou, 516081, China.
Shanzhou HuangDepartment of General Surgery, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, 510080, China. hshanzh@163.com.
Chuanzhao ZhangDepartment of General Surgery, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, 510080, China. zhangchuanzhao@gpdh.org.cn.
Baohua HouDepartment of General Surgery, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, 510080, China. hbh1000@126.com.
Guangdong Provincial People's Hospital · CNGuangdong Academy of Medical Sciences · CNSouth China University of Technology · CNSouthern Medical University · CNThe First Affiliated Hospital, Sun Yat-sen University · CN

Funding

Basic and applied basic research funding of Guangdong Province 2021A1515011473Basic and applied basic research funding of Guangdong Province 2021A1515011577Basic and applied basic research funding of Guangdong Province 2021A1515012441Collaborative Funding of Basic and Applied Basis Research Funding of Guangdong Province 2020A1515110536Funding for the Construction of Key Specialty in Huizhou Qi ZhouNational Natural Science Foundation of China 81672475National Natural Science Foundation of China 82072635National Natural Science Foundation of China 82072637Special Funding from Guangdong Provincial People's Hospital 8200100290Special Funding from Guangdong Provincial People's Hospital KY012021164the Science and Technology Program of Guangzhou 202102020030the Science and Technology Program of Huizhou 2019C0602009the Science and Technology Program of Huizhou Daya Bay 2020030401
6 · The paper itself

Abstract

backgroundPancreatic ductal adenocarcinoma (PDAC) is one of the deadliest cancer due to its highly aggressive phenotype and lack of effective biomarkers or treatment strategies. ZMAT1 belongs to the C2H2 type zinc finger family, but its biological function is rarely investigated, as well as its role in cancer development.

methodsMultiple bioinformatics analyses were used to evaluate ZMAT1 expression and potential role in PDAC. Intro and vivo studies were performed to assess the effects of ZMAT1 on PDAC cells growth. Furthermore, CHIP-seq and luciferase reporter assay was conducted to identify its specific regulatory mechanism in PDAC.

resultsThe current study identified the down-regulation of ZMAT1 and its associations with unfavorable clinicopathological characteristics and poor survival of PDAC. Further, we found overexpression of ZMAT1 inhibited pancreatic cancer cell proliferation by inducing p21, leading to impaired S/G2 cell cycle progression. Besides, over-expression of ZMAT1 led to decreased pancreatic cancer cell apoptosis. Mechanistically, ZMAT1 up-regulated p53 expression and inhibition of p53 abrogated the effect of ZMAT1 over-expression on pancreatic cancer cell, indicating the role of ZMAT1 in PDAC was dependent on p53. By performing CHIP-seq assay, we found ZMAT1 did not bind to P53 but bound to the promoter region of SIRT3, an upstream regulator for p53. Luciferase reporter assay showed transfection of ZMAT1 induced SIRT3 transcription, suggesting ZMAT1 was a transcriptional activator for SIRT3.

conclusionOur findings indicated the role of ZMAT1-SIRT3-p53 signaling pathway during tumor growth, highlighting that ZMAT1 is a tumor suppressor and novel biomarker of PDAC.

Indexed as

Carcinoma, Pancreatic DuctalPancreatic NeoplasmsSirtuin 3Tumor Suppressor Protein p53Cell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticGenes, Tumor SuppressorHumansSignal TransductionSIRT3 protein, humanSirtuin 3TP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID35392973
PMCPMC8988381
OpenAlexW4223545142

What OpenQuestion holds

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LicenceCC BY
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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.