Cargando…
EPA Modulates KLK Genes via miR-378: A Potential Therapy in Prostate Cancer
SIMPLE SUMMARY: Castration resistant prostate cancer (CRPC) is one of the most pestilent form of prostate cancer (PCa), accounting for approximately 10–20% of all PCas, which carry poor mortality and morbidity rates. The focus in this study is on EPA, a natural supplement commonly found in fish oils...
Autores principales: | , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9179265/ https://www.ncbi.nlm.nih.gov/pubmed/35681793 http://dx.doi.org/10.3390/cancers14112813 |
_version_ | 1784723231799771136 |
---|---|
author | Yu, Kai-Jie Ji, De-Yi Hsieh, Ming-Li Chuang, Cheng-Keng Pang, See-Tong Weng, Wen-Hui |
author_facet | Yu, Kai-Jie Ji, De-Yi Hsieh, Ming-Li Chuang, Cheng-Keng Pang, See-Tong Weng, Wen-Hui |
author_sort | Yu, Kai-Jie |
collection | PubMed |
description | SIMPLE SUMMARY: Castration resistant prostate cancer (CRPC) is one of the most pestilent form of prostate cancer (PCa), accounting for approximately 10–20% of all PCas, which carry poor mortality and morbidity rates. The focus in this study is on EPA, a natural supplement commonly found in fish oils. EPA induces the expression of PGC-1β gene and co-expresses miR-378 in cells, a nucleic acid sequence that inhibits PCa cell proliferation. This significance is highlighted in this study as a potential adjunctive therapy for all stages of PCa including CRPC. ABSTRACT: It is known that miRNA-378a-3p (miR-378) could be induced by eicosapentaenoic acid (EPA), an omega-3 fatty acid. Herein, we first demonstrated how miR-378 exerts anti-prostate cancer (PCa) actions by influencing multiple target genes, including KLK2, KLK4, KLK6, and KLK14, which are implicated in PCa development, cell proliferation, and cell survival. Furthermore, these genes also correlate with androgen and mTOR signaling transduction, and are considered pivotal pathways for the onset and progression of PCa. In total, four PCa cell lines and eight pairing tissues (tumor vs. normal) from clinical PCa patients were included in the current study. The results showed high significance after EPA induced tumor cells containing higher expression levels of miR-378, and led the PCa cells having low cell viabilities, and they progressed to apoptosis when compared with normal prostate cells (p < 0.001). The findings indicated that EPA might become a potential therapy for PCa, especially because it is derived from the components of natural fish oil; it may prove to be a great help for solving the problem of castration-resistant prostate cancer (CRPC). |
format | Online Article Text |
id | pubmed-9179265 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-91792652022-06-10 EPA Modulates KLK Genes via miR-378: A Potential Therapy in Prostate Cancer Yu, Kai-Jie Ji, De-Yi Hsieh, Ming-Li Chuang, Cheng-Keng Pang, See-Tong Weng, Wen-Hui Cancers (Basel) Communication SIMPLE SUMMARY: Castration resistant prostate cancer (CRPC) is one of the most pestilent form of prostate cancer (PCa), accounting for approximately 10–20% of all PCas, which carry poor mortality and morbidity rates. The focus in this study is on EPA, a natural supplement commonly found in fish oils. EPA induces the expression of PGC-1β gene and co-expresses miR-378 in cells, a nucleic acid sequence that inhibits PCa cell proliferation. This significance is highlighted in this study as a potential adjunctive therapy for all stages of PCa including CRPC. ABSTRACT: It is known that miRNA-378a-3p (miR-378) could be induced by eicosapentaenoic acid (EPA), an omega-3 fatty acid. Herein, we first demonstrated how miR-378 exerts anti-prostate cancer (PCa) actions by influencing multiple target genes, including KLK2, KLK4, KLK6, and KLK14, which are implicated in PCa development, cell proliferation, and cell survival. Furthermore, these genes also correlate with androgen and mTOR signaling transduction, and are considered pivotal pathways for the onset and progression of PCa. In total, four PCa cell lines and eight pairing tissues (tumor vs. normal) from clinical PCa patients were included in the current study. The results showed high significance after EPA induced tumor cells containing higher expression levels of miR-378, and led the PCa cells having low cell viabilities, and they progressed to apoptosis when compared with normal prostate cells (p < 0.001). The findings indicated that EPA might become a potential therapy for PCa, especially because it is derived from the components of natural fish oil; it may prove to be a great help for solving the problem of castration-resistant prostate cancer (CRPC). MDPI 2022-06-06 /pmc/articles/PMC9179265/ /pubmed/35681793 http://dx.doi.org/10.3390/cancers14112813 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Communication Yu, Kai-Jie Ji, De-Yi Hsieh, Ming-Li Chuang, Cheng-Keng Pang, See-Tong Weng, Wen-Hui EPA Modulates KLK Genes via miR-378: A Potential Therapy in Prostate Cancer |
title | EPA Modulates KLK Genes via miR-378: A Potential Therapy in Prostate Cancer |
title_full | EPA Modulates KLK Genes via miR-378: A Potential Therapy in Prostate Cancer |
title_fullStr | EPA Modulates KLK Genes via miR-378: A Potential Therapy in Prostate Cancer |
title_full_unstemmed | EPA Modulates KLK Genes via miR-378: A Potential Therapy in Prostate Cancer |
title_short | EPA Modulates KLK Genes via miR-378: A Potential Therapy in Prostate Cancer |
title_sort | epa modulates klk genes via mir-378: a potential therapy in prostate cancer |
topic | Communication |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9179265/ https://www.ncbi.nlm.nih.gov/pubmed/35681793 http://dx.doi.org/10.3390/cancers14112813 |
work_keys_str_mv | AT yukaijie epamodulatesklkgenesviamir378apotentialtherapyinprostatecancer AT jideyi epamodulatesklkgenesviamir378apotentialtherapyinprostatecancer AT hsiehmingli epamodulatesklkgenesviamir378apotentialtherapyinprostatecancer AT chuangchengkeng epamodulatesklkgenesviamir378apotentialtherapyinprostatecancer AT pangseetong epamodulatesklkgenesviamir378apotentialtherapyinprostatecancer AT wengwenhui epamodulatesklkgenesviamir378apotentialtherapyinprostatecancer |