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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Autores principales: Patrice Cagle, Suryakant Niture, Anvesha Srivastava, Malathi Ramalinga, Rasha Aqeel, Leslimar Rios-Colon, Uchechukwu Chimeh, Simeng Suy, Sean P. Collins, Rajvir Dahiya, Deepak Kumar
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Publicado: Nature Portfolio 2019
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Acceso en línea:https://doaj.org/article/955ba9b3dedc4b5f87e00625a4479c4a
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spelling 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)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle 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
description 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
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