miR-100-5p inhibition induces apoptosis in dormant prostate cancer cells and prevents the emergence of castration-resistant prostate cancer
Abstract Carcinoma of the prostate is the most common cancer in men. Treatment of aggressive prostate cancer involves a regiment of radical prostectomy, radiation therapy, chemotherapy and hormonal therapy. Despite significant improvements in the last decade, the treatment of prostate cancer remains...
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Nature Portfolio
2017
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oai:doaj.org-article:30400add8b0940e997d768e8615208812021-12-02T12:32:49ZmiR-100-5p inhibition induces apoptosis in dormant prostate cancer cells and prevents the emergence of castration-resistant prostate cancer10.1038/s41598-017-03731-82045-2322https://doaj.org/article/30400add8b0940e997d768e8615208812017-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-03731-8https://doaj.org/toc/2045-2322Abstract Carcinoma of the prostate is the most common cancer in men. Treatment of aggressive prostate cancer involves a regiment of radical prostectomy, radiation therapy, chemotherapy and hormonal therapy. Despite significant improvements in the last decade, the treatment of prostate cancer remains unsatisfactory, because a significant fraction of prostate cancers develop resistance to multiple treatments and become incurable. This prompts an urgent need to investigate the molecular mechanisms underlying the evolution of therapy-induced resistance of prostate cancer either in the form of castration-resistant prostate cancer (CRPC) or transdifferentiated neuroendocrine prostate cancer (NEPC). By analyzing micro-RNA expression profiles in a set of patient-derived prostate cancer xenograft tumor lines, we identified miR-100-5p as one of the key molecular components in the initiation and evolution of androgen ablation therapy resistance in prostate cancer. In vitro results showed that miR-100-5p is required for hormone-independent survival and proliferation of prostate cancer cells post androgen ablation. In Silico target predictions revealed that miR-100-5p target genes are involved in key aspects of cancer progression, and are associated with clinical outcome. Our results suggest that mir-100-5p is a possible therapeutic target involved in prostate cancer progression and relapse post androgen ablation therapy.Noushin NabaviNur Ridzwan Nur SaidyErik VenalainenAnne HaegertAbhijit ParoliaHui XueYuwei WangRebecca WuXin DongColin CollinsFrancesco CreaYuzhuo WangNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-10 (2017) |
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Medicine R Science Q Noushin Nabavi Nur Ridzwan Nur Saidy Erik Venalainen Anne Haegert Abhijit Parolia Hui Xue Yuwei Wang Rebecca Wu Xin Dong Colin Collins Francesco Crea Yuzhuo Wang miR-100-5p inhibition induces apoptosis in dormant prostate cancer cells and prevents the emergence of castration-resistant prostate cancer |
| description |
Abstract Carcinoma of the prostate is the most common cancer in men. Treatment of aggressive prostate cancer involves a regiment of radical prostectomy, radiation therapy, chemotherapy and hormonal therapy. Despite significant improvements in the last decade, the treatment of prostate cancer remains unsatisfactory, because a significant fraction of prostate cancers develop resistance to multiple treatments and become incurable. This prompts an urgent need to investigate the molecular mechanisms underlying the evolution of therapy-induced resistance of prostate cancer either in the form of castration-resistant prostate cancer (CRPC) or transdifferentiated neuroendocrine prostate cancer (NEPC). By analyzing micro-RNA expression profiles in a set of patient-derived prostate cancer xenograft tumor lines, we identified miR-100-5p as one of the key molecular components in the initiation and evolution of androgen ablation therapy resistance in prostate cancer. In vitro results showed that miR-100-5p is required for hormone-independent survival and proliferation of prostate cancer cells post androgen ablation. In Silico target predictions revealed that miR-100-5p target genes are involved in key aspects of cancer progression, and are associated with clinical outcome. Our results suggest that mir-100-5p is a possible therapeutic target involved in prostate cancer progression and relapse post androgen ablation therapy. |
| format |
article |
| author |
Noushin Nabavi Nur Ridzwan Nur Saidy Erik Venalainen Anne Haegert Abhijit Parolia Hui Xue Yuwei Wang Rebecca Wu Xin Dong Colin Collins Francesco Crea Yuzhuo Wang |
| author_facet |
Noushin Nabavi Nur Ridzwan Nur Saidy Erik Venalainen Anne Haegert Abhijit Parolia Hui Xue Yuwei Wang Rebecca Wu Xin Dong Colin Collins Francesco Crea Yuzhuo Wang |
| author_sort |
Noushin Nabavi |
| title |
miR-100-5p inhibition induces apoptosis in dormant prostate cancer cells and prevents the emergence of castration-resistant prostate cancer |
| title_short |
miR-100-5p inhibition induces apoptosis in dormant prostate cancer cells and prevents the emergence of castration-resistant prostate cancer |
| title_full |
miR-100-5p inhibition induces apoptosis in dormant prostate cancer cells and prevents the emergence of castration-resistant prostate cancer |
| title_fullStr |
miR-100-5p inhibition induces apoptosis in dormant prostate cancer cells and prevents the emergence of castration-resistant prostate cancer |
| title_full_unstemmed |
miR-100-5p inhibition induces apoptosis in dormant prostate cancer cells and prevents the emergence of castration-resistant prostate cancer |
| title_sort |
mir-100-5p inhibition induces apoptosis in dormant prostate cancer cells and prevents the emergence of castration-resistant prostate cancer |
| publisher |
Nature Portfolio |
| publishDate |
2017 |
| url |
https://doaj.org/article/30400add8b0940e997d768e861520881 |
| work_keys_str_mv |
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