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PRPF4 is a novel therapeutic target for the treatment of breast cancer by influencing growth, migration, invasion, and apoptosis of breast cancer cells via p38 MAPK signaling pathway

Title
PRPF4 is a novel therapeutic target for the treatment of breast cancer by influencing growth, migration, invasion, and apoptosis of breast cancer cells via p38 MAPK signaling pathway
Authors
Park, SongHan, Se-HyeonKim, Hyeon‐GyeomJeong, JainChoi, MinjeeKim, HeeyeonKim, Min‐GiPark, Jin-KyuHan, Jee EunCho, Gil-JaeKim, Myoung OkRyoo, Zae YoungChoi, Seong-Kyoon
DGIST Authors
Choi, Seong-Kyoon
Issue Date
2019-10
Citation
Molecular and Cellular Probes, 47
Type
Article
Article Type
Article
Author Keywords
PRPF4Breast cancerMetastasisp38 MAPKApoptosis
Keywords
MOLECULAR PORTRAITS14-3-3 PROTEINSKINASEEXPRESSIONREVEALS
ISSN
0890-8508
Abstract
Pre-mRNA processing factor 4 (PRPF4), a core protein in U4/U6 snRNP, maintains snRNP structures by interacting with PRPF3 and cyclophilin H. Expression of the PRPF4 gene affects cell survival as well as apoptosis and is responsible for retinitis pigmentosa (RP). Proteomics analysis shows that PRPF4 may be a therapeutic target in human cancers. Nevertheless, the exact function and role of the PRPF4 gene are unclear. In this study, we assessed the expression of PRPF4 gene in human breast cancer cells. First, we confirmed that the PRPF4 gene was overexpressed in various breast cancer cell lines. Next, using breast cancer cell lines MCF7 and MDA-MB-468, we established stable cell lines with PRPF4 gene knockdown. We also performed microarray analysis to investigate molecular mechanisms underlying PRPF4 activity. All cell lines with PRPF4 gene knockdown exhibited reduced cell proliferation, remarkable reduction in anchorage-independent colony formation capacity, and reduction of PCNA protein, which is a marker cell of proliferation. Reduced expression of the PRPF4 gene induced apoptosis and changes in the expression of associated apoptotic markers in breast cancer cell lines. Knockdown of the PRPF4 gene reduced cellular capacity for migration and invasion (the key hallmarks of human cancers) and decreased the expression of genes involved in epithelial-mesenchymal transition (EMT). Microarray results showed that the expression of PPIP5K1, PPIPK2, and YWHAE genes was reduced at the transcriptional level, leading to reduced phosphorylation of p38 MAPK. These findings suggest that knockdown of PRPF4 gene slows down breast cancer progression via suppression of p38 MAPK phosphorylation. In conclusion, the PRPF4 gene plays an important role in the growth of breast cancer cells and is therefore a potential therapeutic target. © 2019 Elsevier Ltd
URI
http://hdl.handle.net/20.500.11750/10832
DOI
10.1016/j.mcp.2019.101440
Publisher
Academic Press
Related Researcher
Files:
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Collection:
Division of Biotechnology1. Journal Articles


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