Evidence map›Paper›PMID 30922330›Full record

ArticleCell communication and signaling : CCS2019

PRMT5 enhances tumorigenicity and glycolysis in pancreatic cancer via the FBW7/cMyc axis.

Yi Qin, Qiangsheng Hu, Jin Xu, Shunrong Ji, Weixing Dai, Wensheng Liu, Wenyan Xu, Qiqing Sun, Zheng Zhang, Quanxing Ni and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed, 1 pooled it
4.7field-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

73 citing papers in PubMed, 1 synthesis or guideline pooled it, 109 citations in OpenAlex.

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  20. Molecular insights and clinical implications for the tumor suppressor role of SCFBiochimica et biophysica acta. Reviews on cancer · 2024
    Review

13 more citing papers are in PubMed but not listed here.

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

13 authors at 2 institutions in 1 country.

Yi QinDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Qiangsheng HuDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Jin XuDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Shunrong JiDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Weixing DaiCancer Research Institute, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Wensheng LiuDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Wenyan XuDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Qiqing SunDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Zheng ZhangDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Quanxing NiDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Bo ZhangDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Xianjun YuDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China. yuxianjun@fudanpci.org.ORCID 0000-0002-6697-7143
Xiaowu XuDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China. xuxiaowu@fudanpci.org.
Shanghai Medical College of Fudan University · CNFudan University Shanghai Cancer Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe epigenetic factor protein arginine methyltransferase 5 (PRMT5) has been reported to play vital roles in a wide range of cellular processes, such as gene transcription, genomic organization, differentiation and cell cycle control. However, its role in pancreatic cancer remains unclear. Our study aimed to investigate the roles of PRMT5 in pancreatic cancer prognosis and progression and to explore the underlying molecular mechanism.

methodsReal-time PCR, immunohistochemistry and analysis of a dataset from The Cancer Genome Atlas (TCGA) were performed to study the expression of PRMT5 at the mRNA and protein levels in pancreatic cancer. Cell proliferation assays, including cell viability, colony formation ability and subcutaneous mouse model assays, were utilized to confirm the role of PRMT5 in cell proliferation and tumorigenesis. A Seahorse extracellular flux analyzer, a glucose uptake kit, a lactate level measurement kit and the measurement of

resultsPRMT5 expression was significantly upregulated in pancreatic cancer tissues compared with that in adjacent normal tissues. Clinically, elevated expression of PRMT5 was positively correlated with worse overall survival in pancreatic cancer patients. Silencing PRMT5 expression inhibited the proliferation of pancreatic cancer cells both in vitro and in vivo. Moreover, PRMT5 regulated aerobic glycolysis in vitro in cell lines, in vivo in pancreatic cancer patients and in a xenograft mouse model used to measure 18F-FDG uptake. We found that mechanistically, PRMT5 posttranslationally regulated cMyc stability via F-box/WD repeat-containing protein 7 (FBW7), an E3 ubiquitin ligase that controls cMyc degradation. Moreover, PRMT5 epigenetically regulated the expression of FBW7 in pancreatic cancer cells.

conclusionsThe present study demonstrated that PRMT5 epigenetically silenced the expression of the tumor suppressor FBW7, leading to increased cMyc levels and the subsequent enhancement of the proliferation of and aerobic glycolysis in pancreatic cancer cells. The PRMT5/FBW7/cMyc axis could be a potential therapeutic target for the treatment of pancreatic cancer.

Indexed as

AnimalsCarcinogenesisCell Line, TumorCell ProliferationCell RespirationEpigenesis, GeneticF-Box-WD Repeat-Containing Protein 7GlycolysisHumansMice, Inbred BALB CPancreatic NeoplasmsProtein-Arginine N-MethyltransferasesProto-Oncogene Proteins c-mycF-Box-WD Repeat-Containing Protein 7FBXW7 protein, humanMYC protein, humanPRMT5 protein, humanProtein-Arginine N-MethyltransferasesProto-Oncogene Proteins c-mycAerobic glycolysiscMycFBW7Pancreatic cancerPRMT5

Identifiers

PMID30922330
PMCPMC6440122
OpenAlexW2945917101

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.