MicroRNA-214 targets PTK6 to inhibit tumorigenic potential and increase drug sensitivity of prostate cancer cells
Abstract Prostate cancer is the most commonly diagnosed cancer in men with African American men disproportionally suffering from the burden of this disease. Biomarkers that could discriminate indolent from aggressive and drug resistance disease are lacking. MicroRNAs are small non-coding RNAs that a...
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Nature Portfolio
2019
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oai:doaj.org-article:955ba9b3dedc4b5f87e00625a4479c4a2021-12-02T15:09:47ZMicroRNA-214 targets PTK6 to inhibit tumorigenic potential and increase drug sensitivity of prostate cancer cells10.1038/s41598-019-46170-32045-2322https://doaj.org/article/955ba9b3dedc4b5f87e00625a4479c4a2019-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-019-46170-3https://doaj.org/toc/2045-2322Abstract Prostate cancer is the most commonly diagnosed cancer in men with African American men disproportionally suffering from the burden of this disease. Biomarkers that could discriminate indolent from aggressive and drug resistance disease are lacking. MicroRNAs are small non-coding RNAs that affect numerous physiological and pathological processes, including cancer development and have been suggested as biomarkers and therapeutic targets. In the present study, we investigated the role of miR-214 on prostate cancer cell survival/migration/invasion, cell cycle regulation, and apoptosis. miR-214 was differentially expressed between Caucasian and African American prostate cancer cells. Importantly, miR-214 overexpression in prostate cancer cells induced apoptosis, inhibiting cell proliferation and colony forming ability. miR-214 expression in prostate cancer cells also inhibited cell migration and 3D spheroid invasion. Mechanistically, miR-214 inhibited prostate cancer cell proliferation by targeting protein tyrosine kinase 6 (PTK6). Restoration of PTK6 expression attenuated the inhibitory effect of miR-214 on cell proliferation. Moreover, simultaneous inhibition of PTK6 by ibrutinib and miR-214 significantly reduced cell proliferation/survival. Our data indicates that miR-214 could act as a tumor suppressor in prostate cancer and could potentially be utilized as a biomarker and therapeutic target.Patrice CagleSuryakant NitureAnvesha SrivastavaMalathi RamalingaRasha AqeelLeslimar Rios-ColonUchechukwu ChimehSimeng SuySean P. CollinsRajvir DahiyaDeepak KumarNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 9, Iss 1, Pp 1-13 (2019) |
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Medicine R Science Q Patrice Cagle Suryakant Niture Anvesha Srivastava Malathi Ramalinga Rasha Aqeel Leslimar Rios-Colon Uchechukwu Chimeh Simeng Suy Sean P. Collins Rajvir Dahiya Deepak Kumar MicroRNA-214 targets PTK6 to inhibit tumorigenic potential and increase drug sensitivity of prostate cancer cells |
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Abstract Prostate cancer is the most commonly diagnosed cancer in men with African American men disproportionally suffering from the burden of this disease. Biomarkers that could discriminate indolent from aggressive and drug resistance disease are lacking. MicroRNAs are small non-coding RNAs that affect numerous physiological and pathological processes, including cancer development and have been suggested as biomarkers and therapeutic targets. In the present study, we investigated the role of miR-214 on prostate cancer cell survival/migration/invasion, cell cycle regulation, and apoptosis. miR-214 was differentially expressed between Caucasian and African American prostate cancer cells. Importantly, miR-214 overexpression in prostate cancer cells induced apoptosis, inhibiting cell proliferation and colony forming ability. miR-214 expression in prostate cancer cells also inhibited cell migration and 3D spheroid invasion. Mechanistically, miR-214 inhibited prostate cancer cell proliferation by targeting protein tyrosine kinase 6 (PTK6). Restoration of PTK6 expression attenuated the inhibitory effect of miR-214 on cell proliferation. Moreover, simultaneous inhibition of PTK6 by ibrutinib and miR-214 significantly reduced cell proliferation/survival. Our data indicates that miR-214 could act as a tumor suppressor in prostate cancer and could potentially be utilized as a biomarker and therapeutic target. |
format |
article |
author |
Patrice Cagle Suryakant Niture Anvesha Srivastava Malathi Ramalinga Rasha Aqeel Leslimar Rios-Colon Uchechukwu Chimeh Simeng Suy Sean P. Collins Rajvir Dahiya Deepak Kumar |
author_facet |
Patrice Cagle Suryakant Niture Anvesha Srivastava Malathi Ramalinga Rasha Aqeel Leslimar Rios-Colon Uchechukwu Chimeh Simeng Suy Sean P. Collins Rajvir Dahiya Deepak Kumar |
author_sort |
Patrice Cagle |
title |
MicroRNA-214 targets PTK6 to inhibit tumorigenic potential and increase drug sensitivity of prostate cancer cells |
title_short |
MicroRNA-214 targets PTK6 to inhibit tumorigenic potential and increase drug sensitivity of prostate cancer cells |
title_full |
MicroRNA-214 targets PTK6 to inhibit tumorigenic potential and increase drug sensitivity of prostate cancer cells |
title_fullStr |
MicroRNA-214 targets PTK6 to inhibit tumorigenic potential and increase drug sensitivity of prostate cancer cells |
title_full_unstemmed |
MicroRNA-214 targets PTK6 to inhibit tumorigenic potential and increase drug sensitivity of prostate cancer cells |
title_sort |
microrna-214 targets ptk6 to inhibit tumorigenic potential and increase drug sensitivity of prostate cancer cells |
publisher |
Nature Portfolio |
publishDate |
2019 |
url |
https://doaj.org/article/955ba9b3dedc4b5f87e00625a4479c4a |
work_keys_str_mv |
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