Identification and Biological Evaluation of a Novel CLK4 Inhibitor Targeting Alternative Splicing in Pancreatic Cancer Using Structure‐Based Virtual Screening

Abstract Pancreatic cancer is an aggressive malignancy with a poor prognosis and limited treatment options. Cdc‐like kinase 4 (CLK4), a kinase that regulates alternative splicing by phosphorylating spliceosome components, is implicated in aberrant splicing events driving pancreatic cancer progressio...

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Main Authors: Chun‐Lin Yang, Yi‐Wen Wu, Huang‐Ju Tu, Yun‐Hsuan Yeh, Tony Eight Lin, Tzu‐Ying Sung, Mu‐Chun Li, Shih‐Chung Yen, Jui‐Hua Hsieh, Ming‐Chin Yu, Sen‐Yung Hsieh, Hsing‐Pang Hsieh, Shiow‐Lin Pan, Kai‐Cheng Hsu
Format: Article
Language:English
Published: Wiley 2025-05-01
Series:Advanced Science
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Online Access:https://doi.org/10.1002/advs.202416323
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author Chun‐Lin Yang
Yi‐Wen Wu
Huang‐Ju Tu
Yun‐Hsuan Yeh
Tony Eight Lin
Tzu‐Ying Sung
Mu‐Chun Li
Shih‐Chung Yen
Jui‐Hua Hsieh
Ming‐Chin Yu
Sen‐Yung Hsieh
Hsing‐Pang Hsieh
Shiow‐Lin Pan
Kai‐Cheng Hsu
author_facet Chun‐Lin Yang
Yi‐Wen Wu
Huang‐Ju Tu
Yun‐Hsuan Yeh
Tony Eight Lin
Tzu‐Ying Sung
Mu‐Chun Li
Shih‐Chung Yen
Jui‐Hua Hsieh
Ming‐Chin Yu
Sen‐Yung Hsieh
Hsing‐Pang Hsieh
Shiow‐Lin Pan
Kai‐Cheng Hsu
author_sort Chun‐Lin Yang
collection DOAJ
description Abstract Pancreatic cancer is an aggressive malignancy with a poor prognosis and limited treatment options. Cdc‐like kinase 4 (CLK4), a kinase that regulates alternative splicing by phosphorylating spliceosome components, is implicated in aberrant splicing events driving pancreatic cancer progression. In this study, we established a computational model that integrates pharmacological interactions of CLK4 inhibitors with an improved hit rate. Through this model, we identified a novel CLK4 inhibitor, compound 150441, with a 50% inhibitory concentration (IC50) value of 21.4 nm. Structure‐activity relationship analysis was performed to investigate key interactions and functional groups. Kinase profiling revealed that compound 150441 is selective for CLK4. Subsequent in vitro assays demonstrated that this inhibitor effectively suppressed cell growth and viability of pancreatic cancer cells. In addition, it inhibited the phosphorylation of key splicing factors, including serine‐ and arginine‐rich splicing factor (SRSF) 4 and SRSF6. Cell cycle analysis further indicated that the compound induced G2/M arrest, leading to apoptosis. RNA‐seq analysis revealed that the compound induced significant changes in alternative splicing and key biological pathways, including RNA processing, DNA replication, DNA damage, and mitosis. These findings suggest that compound 150441 has promising potential for further development as a novel pancreatic cancer treatment.
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spelling doaj-art-3a7ba31d767b4dd0acb99416eead9ced2025-08-20T02:26:18ZengWileyAdvanced Science2198-38442025-05-011219n/an/a10.1002/advs.202416323Identification and Biological Evaluation of a Novel CLK4 Inhibitor Targeting Alternative Splicing in Pancreatic Cancer Using Structure‐Based Virtual ScreeningChun‐Lin Yang0Yi‐Wen Wu1Huang‐Ju Tu2Yun‐Hsuan Yeh3Tony Eight Lin4Tzu‐Ying Sung5Mu‐Chun Li6Shih‐Chung Yen7Jui‐Hua Hsieh8Ming‐Chin Yu9Sen‐Yung Hsieh10Hsing‐Pang Hsieh11Shiow‐Lin Pan12Kai‐Cheng Hsu13Graduate Institute of Cancer Biology and Drug Discovery College of Medical Science and Technology Taipei Medical University Taipei 110301 TaiwanGraduate Institute of Cancer Biology and Drug Discovery College of Medical Science and Technology Taipei Medical University Taipei 110301 TaiwanGraduate Institute of Cancer Biology and Drug Discovery College of Medical Science and Technology Taipei Medical University Taipei 110301 TaiwanGraduate Institute of Cancer Biology and Drug Discovery College of Medical Science and Technology Taipei Medical University Taipei 110301 TaiwanGraduate Institute of Cancer Biology and Drug Discovery College of Medical Science and Technology Taipei Medical University Taipei 110301 TaiwanGraduate Institute of Cancer Biology and Drug Discovery College of Medical Science and Technology Taipei Medical University Taipei 110301 TaiwanInstitute of Biotechnology and Pharmaceutical Research National Health Research Institutes Miaoli County 350401 TaiwanWarshel Institute for Computational Biology School of Medicine The Chinese University of Hong Kong (Shenzhen) Shenzhen Guangdong 518172 ChinaDivision of Translational Toxicology National Institute of Environmental Health Sciences National Institutes of Health Durham NC 27709 USACollege of Medicine Chang Gung University Taoyuan 333323 TaiwanCollege of Medicine Chang Gung University Taoyuan 333323 TaiwanInstitute of Biotechnology and Pharmaceutical Research National Health Research Institutes Miaoli County 350401 TaiwanGraduate Institute of Cancer Biology and Drug Discovery College of Medical Science and Technology Taipei Medical University Taipei 110301 TaiwanGraduate Institute of Cancer Biology and Drug Discovery College of Medical Science and Technology Taipei Medical University Taipei 110301 TaiwanAbstract Pancreatic cancer is an aggressive malignancy with a poor prognosis and limited treatment options. Cdc‐like kinase 4 (CLK4), a kinase that regulates alternative splicing by phosphorylating spliceosome components, is implicated in aberrant splicing events driving pancreatic cancer progression. In this study, we established a computational model that integrates pharmacological interactions of CLK4 inhibitors with an improved hit rate. Through this model, we identified a novel CLK4 inhibitor, compound 150441, with a 50% inhibitory concentration (IC50) value of 21.4 nm. Structure‐activity relationship analysis was performed to investigate key interactions and functional groups. Kinase profiling revealed that compound 150441 is selective for CLK4. Subsequent in vitro assays demonstrated that this inhibitor effectively suppressed cell growth and viability of pancreatic cancer cells. In addition, it inhibited the phosphorylation of key splicing factors, including serine‐ and arginine‐rich splicing factor (SRSF) 4 and SRSF6. Cell cycle analysis further indicated that the compound induced G2/M arrest, leading to apoptosis. RNA‐seq analysis revealed that the compound induced significant changes in alternative splicing and key biological pathways, including RNA processing, DNA replication, DNA damage, and mitosis. These findings suggest that compound 150441 has promising potential for further development as a novel pancreatic cancer treatment.https://doi.org/10.1002/advs.202416323alternative splicingCLK4kinase inhibitorpancreatic cancerstructure‐based virtual screening
spellingShingle Chun‐Lin Yang
Yi‐Wen Wu
Huang‐Ju Tu
Yun‐Hsuan Yeh
Tony Eight Lin
Tzu‐Ying Sung
Mu‐Chun Li
Shih‐Chung Yen
Jui‐Hua Hsieh
Ming‐Chin Yu
Sen‐Yung Hsieh
Hsing‐Pang Hsieh
Shiow‐Lin Pan
Kai‐Cheng Hsu
Identification and Biological Evaluation of a Novel CLK4 Inhibitor Targeting Alternative Splicing in Pancreatic Cancer Using Structure‐Based Virtual Screening
Advanced Science
alternative splicing
CLK4
kinase inhibitor
pancreatic cancer
structure‐based virtual screening
title Identification and Biological Evaluation of a Novel CLK4 Inhibitor Targeting Alternative Splicing in Pancreatic Cancer Using Structure‐Based Virtual Screening
title_full Identification and Biological Evaluation of a Novel CLK4 Inhibitor Targeting Alternative Splicing in Pancreatic Cancer Using Structure‐Based Virtual Screening
title_fullStr Identification and Biological Evaluation of a Novel CLK4 Inhibitor Targeting Alternative Splicing in Pancreatic Cancer Using Structure‐Based Virtual Screening
title_full_unstemmed Identification and Biological Evaluation of a Novel CLK4 Inhibitor Targeting Alternative Splicing in Pancreatic Cancer Using Structure‐Based Virtual Screening
title_short Identification and Biological Evaluation of a Novel CLK4 Inhibitor Targeting Alternative Splicing in Pancreatic Cancer Using Structure‐Based Virtual Screening
title_sort identification and biological evaluation of a novel clk4 inhibitor targeting alternative splicing in pancreatic cancer using structure based virtual screening
topic alternative splicing
CLK4
kinase inhibitor
pancreatic cancer
structure‐based virtual screening
url https://doi.org/10.1002/advs.202416323
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