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Open AccessArticle
Modulation of PRC1 Promotes Anticancer Effects in Pancreatic Cancer
by
Hajin Lee
Hajin Lee ,
An-Na Bae
An-Na Bae ,
Huiseong Yang
Huiseong Yang ,
Jae-Ho Lee
Jae-Ho Lee
Prof. Dr. Jae-Ho Lee obtained his degree in Medicine in 2007 and received his doctorate in Anatomy a [...]
Prof. Dr. Jae-Ho Lee obtained his degree in Medicine in 2007 and received his doctorate in Anatomy with Clinical Anatomy and Cancer Molecular Genetics as two sub-specialties from Keimyung University School of Medicine in 2013. After graduation, he moved to Yonsei University School of Medicine as a postdoctoral fellow for one year. He then returned to Keimyung University School of Medicine as an Assistant Professor. He was awarded the 2014 Award of President PostDoc Fellowship by the National Research Foundation and Best Article Awards for young researchers from the Professor Association in Keimyung University School of Medicine in 2014 and 2016. He is on the Editorial Board of the Medicine journal and the Reviewer board of the Korean Journal of Physical Anthropology. His main research areas include anatomical variation, molecular biology, and translational research in cancers.
and
Jong Ho Park
Jong Ho Park *
Department of Anatomy, School of Medicine, Keimyung University, Daegu 42601, Republic of Korea
*
Author to whom correspondence should be addressed.
Submission received: 5 August 2024
/
Revised: 11 September 2024
/
Accepted: 25 September 2024
/
Published: 27 September 2024
Simple Summary
Protein Regulator of Cytokinesis (PRC) 1 is traditionally recognized for its role in the final physical stage of cell division. However, recent studies have highlighted its significant involvement in various cancers. This study aimed to assess the clinical relevance of PRC1 in pancreatic cancer and its impact on cancer cell characteristics. Based on data from The Cancer Genome Atlas (TCGA) and a cell-based assay, PRC1 has emerged as a clinical marker for pancreatic cancer. These findings suggest that the regulation of PRC1 provides a promising strategy for developing anticancer therapies in pancreatic cancer.
Abstract
Background: Pancreatic cancer, while relatively uncommon, is extrapolated to become the second leading cause of cancer-related deaths worldwide. Despite identifying well-known markers like the KRAS gene, the exact regulation of pancreatic cancer progression remains elusive. Methods: Clinical value of PRC1 was analyzed using bioinformatics database. The role of PRC1 was further evaluated through cell-based assays, including viability, wound healing, and sensitivity with the drug. Results: We demonstrate that PRC1 was significantly overexpressed in pancreatic cancer compared to pancreases without cancer, as revealed through human databases and cell lines analysis. Furthermore, high PRC1 expression had a negative correlation with CD4+ T cells, which are crucial for the immune response against cancers. Additionally, PRC1 showed a positive correlation with established pancreatic cancer markers. Silencing PRC1 expression using siRNA significantly inhibited cancer cell proliferation and viability and increased chemotherapeutic drug sensitivity. Conclusions: These findings suggest that targeting PRC1 in pancreatic cancer may enhance immune cell infiltration and inhibit cancer cell proliferation, offering a promising avenue for developing anticancer therapies.
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MDPI and ACS Style
Lee, H.; Bae, A.-N.; Yang, H.; Lee, J.-H.; Park, J.H.
Modulation of PRC1 Promotes Anticancer Effects in Pancreatic Cancer. Cancers 2024, 16, 3310.
https://doi.org/10.3390/cancers16193310
AMA Style
Lee H, Bae A-N, Yang H, Lee J-H, Park JH.
Modulation of PRC1 Promotes Anticancer Effects in Pancreatic Cancer. Cancers. 2024; 16(19):3310.
https://doi.org/10.3390/cancers16193310
Chicago/Turabian Style
Lee, Hajin, An-Na Bae, Huiseong Yang, Jae-Ho Lee, and Jong Ho Park.
2024. "Modulation of PRC1 Promotes Anticancer Effects in Pancreatic Cancer" Cancers 16, no. 19: 3310.
https://doi.org/10.3390/cancers16193310
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