Evidence map›Paper›PMID 31775892›Full record

ArticleJournal of experimental & clinical cancer research : CR2019

MFAP5 facilitates the aggressiveness of intrahepatic Cholangiocarcinoma by activating the Notch1 signaling pathway.

Jian-Hui Li, Xiao-Xu Zhu, Fu-Xi Li, Chen-Song Huang, Xi-Tai Huang, Jie-Qin Wang, Zhuo-Xing Gao, Shi-Jin Li, Qiong-Cong Xu, Wei Zhao and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

29 citing papers in PubMed, 45 citations in OpenAlex.

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  5. Loss of MFAP5 and Its Effect on Skin Homeostasis and Wound Healing.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 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

11 authors at 1 institution in 1 country.

Jian-Hui LiDepartment of Pancreato-Biliary Surgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080, China.
Xiao-Xu ZhuDepartment of Pancreato-Biliary Surgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080, China.
Fu-Xi LiKey Laboratory of Stem Cells and Tissue Engineering (Sun Yat-Sen University), Ministry of Education, Guangzhou, 510080, China.
Chen-Song HuangDepartment of Pancreato-Biliary Surgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080, China.
Xi-Tai HuangDepartment of Pancreato-Biliary Surgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080, China.
Jie-Qin WangDepartment of Pancreato-Biliary Surgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080, China.
Zhuo-Xing GaoKey Laboratory of Stem Cells and Tissue Engineering (Sun Yat-Sen University), Ministry of Education, Guangzhou, 510080, China.
Shi-Jin LiDepartment of Pancreato-Biliary Surgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080, China.
Qiong-Cong XuDepartment of Pancreato-Biliary Surgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080, China.
Wei ZhaoKey Laboratory of Stem Cells and Tissue Engineering (Sun Yat-Sen University), Ministry of Education, Guangzhou, 510080, China. zhaowei23@mail.sysu.edu.cn.
Xiao-Yu YinDepartment of Pancreato-Biliary Surgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080, China. yinxy@mail.sysu.edu.cn.ORCID http://orcid.org/0000-0002-5578-3407
Sun Yat-sen University · CN

Funding

Guangdong Innovative and Entrepreneurial Research Team Program 2016ZT06S029National Natural Science Foundation of China 31771630National Natural Science Foundation of China 81472261National Natural Science Foundation of China 81572766National Natural Science Foundation of China 81772522Natural Science Foundation of Guangdong Province 2016A030313238Natural Science Foundation of Guangdong Province 2017A030312009Natural Science Foundation of Guangdong Province 2019A1515010686Postdoctoral Research Foundation of China 2016M602588Postdoctoral Research Foundation of China 2108M643325Postdoctoral Research Foundation of China 2108M643327Science and Technology Development Projects of Guangzhou, Guangdong, China 201604020044Shenzhen Science Foundation KY20160309
6 · The paper itself

Abstract

backgroundIntrahepatic cholangiocarcinoma (ICC) is the second most common primary liver cancer. The dismal outcome of ICC patients is due to lack of early diagnosis, the aggressive biological behavior of ICC and the lack of effective therapeutic options. Early diagnosis and prognosis of ICC by non-invasive methods would be helpful in providing valuable information and developing effective treatment strategies.

methodsExpression of microfibrillar-associated protein 5 (MFAP5) in the serum of ICC patients was detected by ELISA. Human ICC specimens were immunostained by MFAP5 antibodies. The growth rate of human ICC cell lines treated with MFAP5 or MFAP5 shRNAs was examined by CCK8 and colony formation assays. Cell cycle analysis was performed with PI staining. The effect of MFAP5 inhibition was assessed by xenograft models in nude mice. RNA-seq and ATAC-seq analyses were used to dissect the molecular mechanism by which MFAP5 promoted ICC aggressiveness.

resultsWe identified MFAP5 as a biomarker for the diagnosis and prognosis of ICC. Upregulated MFAP5 is a common feature in aggressive ICC patients' tissues. Importantly, MFAP5 level in the serum of ICC patients and healthy individuals showed significant differential expression profiles. Furthermore, we showed that MFAP5 promoted ICC cell growth and G1 to S-phase transition. Using RNA-seq expression and ATAC-seq chromatin accessibility profiling of ICC cells with suppressed MFAP5 secretion, we showed that MFAP5 regulated the expression of genes involved in the Notch1 signaling pathway. Furthermore, FLI-06, a Notch signaling inhibitor, completely abolished the MFAP5-dependent transcriptional programs.

conclusionsRaised MFAP5 serum level is useful for differentiating ICC patients from healthy individuals, and could be helpful in ICC diagnosis, prognosis and therapies.

Indexed as

Bile Duct NeoplasmsBiomarkers, TumorCase-Control StudiesCell Growth ProcessesCholangiocarcinomaContractile ProteinsHumansIntercellular Signaling Peptides and ProteinsReceptor, Notch1Signal TransductionTranscriptomeTransfectionBiomarkers, TumorContractile ProteinsIntercellular Signaling Peptides and ProteinsMFAP5 protein, humanNOTCH1 protein, humanReceptor, Notch1Cancer biomarkersCell cycle arrestIntrahepatic cholangiocarcinomaMFAP5NOTCH

Identifiers

PMID31775892
PMCPMC6882185
OpenAlexW2989872161

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.