PRMT5 Promotes Pancreatic Cancer Tumorigenesis via Positive PRMT5/C‐Myc Feedback Loop

ABSTRACT The oncogenic role and underlying mechanism of PRMT5 in pancreatic ductal adenocarcinoma (PAAD) remained to be elucidated. In this study, we aimed to investigate the oncogenic role, underlying molecular mechanisms, and potential therapeutic value of PRMT5 in PAAD. PRMT5 was significantly up...

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Main Authors: Fan Yang, Ping Song, Zhaofeng Xiao, Renyi Su, Xin Fang, Yichao Wu, Xiao Xu, Kai Wang
Format: Article
Language:English
Published: Wiley 2025-06-01
Series:MedComm
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Online Access:https://doi.org/10.1002/mco2.70150
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author Fan Yang
Ping Song
Zhaofeng Xiao
Renyi Su
Xin Fang
Yichao Wu
Xiao Xu
Kai Wang
author_facet Fan Yang
Ping Song
Zhaofeng Xiao
Renyi Su
Xin Fang
Yichao Wu
Xiao Xu
Kai Wang
author_sort Fan Yang
collection DOAJ
description ABSTRACT The oncogenic role and underlying mechanism of PRMT5 in pancreatic ductal adenocarcinoma (PAAD) remained to be elucidated. In this study, we aimed to investigate the oncogenic role, underlying molecular mechanisms, and potential therapeutic value of PRMT5 in PAAD. PRMT5 was significantly upregulated in pancreatic cancer than adjacent nontumor pancreas, which was positively correlated with poor prognosis. Genetic and pharmacological inhibition of PRMT5 suppressed PAAD proliferation in vitro and in vivo, exhibiting promising therapeutic effect in vivo. Mechanistically, PRMT5 directly bound to the promoter region of c‐Myc and activated its transcription. Transcriptionally activated c‐Myc in turn inhibited proteasome‐mediated degradation of PRMT5 and enhanced its protein stability, resulting in increased PRMT5 expression. The maintained PRMT5 further enhanced the transcription of c‐Myc. In conclusion, PRMT5 forms a positive feedback loop with c‐Myc to promote the proliferation of pancreatic cancer. Targeting this oncogenic communication may represent a novel and potential therapeutic approach for pancreatic cancer.
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institution Kabale University
issn 2688-2663
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publishDate 2025-06-01
publisher Wiley
record_format Article
series MedComm
spelling doaj-art-382a5bba2197481e8f0d49d0b0ed0aa52025-08-20T03:39:28ZengWileyMedComm2688-26632025-06-0166n/an/a10.1002/mco2.70150PRMT5 Promotes Pancreatic Cancer Tumorigenesis via Positive PRMT5/C‐Myc Feedback LoopFan Yang0Ping Song1Zhaofeng Xiao2Renyi Su3Xin Fang4Yichao Wu5Xiao Xu6Kai Wang7Department of Vascular Surgery Affiliated Hangzhou First People's Hospital School of Medicine Westlake University Hangzhou ChinaDepartment of Gastroenterology Affiliated Hangzhou First People's Hospital School of Medicine Westlake University Hangzhou ChinaThe Fourth School of Clinical Medicine Zhejiang Chinese Medical University Hangzhou ChinaSchool of Clinical Medicine Zhejiang University Hangzhou ChinaDepartment of Vascular Surgery Affiliated Hangzhou First People's Hospital School of Medicine Westlake University Hangzhou ChinaDepartment of Hepatobiliary Pancreatic and Minimal Invasive Surgery Zhejiang Provincial People's Hospital (Affiliated People's Hospital) Hangzhou Medical College Hangzhou ChinaDepartment of Hepatobiliary Pancreatic and Minimal Invasive Surgery Zhejiang Provincial People's Hospital (Affiliated People's Hospital) Hangzhou Medical College Hangzhou ChinaSchool of Clinical Medicine Hangzhou Medical College Hangzhou ChinaABSTRACT The oncogenic role and underlying mechanism of PRMT5 in pancreatic ductal adenocarcinoma (PAAD) remained to be elucidated. In this study, we aimed to investigate the oncogenic role, underlying molecular mechanisms, and potential therapeutic value of PRMT5 in PAAD. PRMT5 was significantly upregulated in pancreatic cancer than adjacent nontumor pancreas, which was positively correlated with poor prognosis. Genetic and pharmacological inhibition of PRMT5 suppressed PAAD proliferation in vitro and in vivo, exhibiting promising therapeutic effect in vivo. Mechanistically, PRMT5 directly bound to the promoter region of c‐Myc and activated its transcription. Transcriptionally activated c‐Myc in turn inhibited proteasome‐mediated degradation of PRMT5 and enhanced its protein stability, resulting in increased PRMT5 expression. The maintained PRMT5 further enhanced the transcription of c‐Myc. In conclusion, PRMT5 forms a positive feedback loop with c‐Myc to promote the proliferation of pancreatic cancer. Targeting this oncogenic communication may represent a novel and potential therapeutic approach for pancreatic cancer.https://doi.org/10.1002/mco2.70150pancreatic cancerPRMT5c‐Mycpositive feedback loopproliferationtherapeutic targets
spellingShingle Fan Yang
Ping Song
Zhaofeng Xiao
Renyi Su
Xin Fang
Yichao Wu
Xiao Xu
Kai Wang
PRMT5 Promotes Pancreatic Cancer Tumorigenesis via Positive PRMT5/C‐Myc Feedback Loop
MedComm
pancreatic cancer
PRMT5
c‐Myc
positive feedback loop
proliferation
therapeutic targets
title PRMT5 Promotes Pancreatic Cancer Tumorigenesis via Positive PRMT5/C‐Myc Feedback Loop
title_full PRMT5 Promotes Pancreatic Cancer Tumorigenesis via Positive PRMT5/C‐Myc Feedback Loop
title_fullStr PRMT5 Promotes Pancreatic Cancer Tumorigenesis via Positive PRMT5/C‐Myc Feedback Loop
title_full_unstemmed PRMT5 Promotes Pancreatic Cancer Tumorigenesis via Positive PRMT5/C‐Myc Feedback Loop
title_short PRMT5 Promotes Pancreatic Cancer Tumorigenesis via Positive PRMT5/C‐Myc Feedback Loop
title_sort prmt5 promotes pancreatic cancer tumorigenesis via positive prmt5 c myc feedback loop
topic pancreatic cancer
PRMT5
c‐Myc
positive feedback loop
proliferation
therapeutic targets
url https://doi.org/10.1002/mco2.70150
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