miR-25 promotes glioma cell proliferation by targeting CDKN1C
MicroRNAs (miRNA) have oncogenic or tumor-suppressive roles in the development and growth of human glioma. Glioma development is also associated with alteration in the activities and expression of cell cycle regulators, and miRNAs are emerging as important regulators of cell cycle progression. Here,...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Zhang, Jihong [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2015transfer abstract |
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| Schlagwörter: |
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| Umfang: |
8 |
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| Übergeordnetes Werk: |
Enthalten in: A Scoping Review of Registered Clinical Trials of Cellular Therapy for COVID-19 and a - Liao, Gary ELSEVIER, 2020, Amsterdam [u.a.] |
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| Übergeordnetes Werk: |
volume:71 ; year:2015 ; pages:7-14 ; extent:8 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.biopha.2015.02.005 |
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| 520 | |a MicroRNAs (miRNA) have oncogenic or tumor-suppressive roles in the development and growth of human glioma. Glioma development is also associated with alteration in the activities and expression of cell cycle regulators, and miRNAs are emerging as important regulators of cell cycle progression. Here, we show that miR-25 is overexpressed in 91% of examined human glioma tissues and 4 out of 6 human glioma cell lines. MiR-25 increases cell proliferation in two independent glioma cell lines. Ectopic expression of miR-25 was found to reduce CDKN1C protein levels by directly targeting its 3′-untranslated region (UTR). Notably, ablation of endogenous miR-25 rescued CDKN1C expression and significantly decreased glioma cell proliferation by facilitating normal cell cycle progression. Our clinical investigation found CDKN1C and miR-25 levels were inversely correlated. Lastly, downregulation of CDKN1 by siRNA blocked the activity of miR-25 on promoting glioma cell proliferation. Overall, our results for the first time show an oncogenic role of miR-25 in human glioma by targeting CDKN1C and that miR-25 could potentially be a therapeutic target for glioma intervention. | ||
| 520 | |a MicroRNAs (miRNA) have oncogenic or tumor-suppressive roles in the development and growth of human glioma. Glioma development is also associated with alteration in the activities and expression of cell cycle regulators, and miRNAs are emerging as important regulators of cell cycle progression. Here, we show that miR-25 is overexpressed in 91% of examined human glioma tissues and 4 out of 6 human glioma cell lines. MiR-25 increases cell proliferation in two independent glioma cell lines. Ectopic expression of miR-25 was found to reduce CDKN1C protein levels by directly targeting its 3′-untranslated region (UTR). Notably, ablation of endogenous miR-25 rescued CDKN1C expression and significantly decreased glioma cell proliferation by facilitating normal cell cycle progression. Our clinical investigation found CDKN1C and miR-25 levels were inversely correlated. Lastly, downregulation of CDKN1 by siRNA blocked the activity of miR-25 on promoting glioma cell proliferation. Overall, our results for the first time show an oncogenic role of miR-25 in human glioma by targeting CDKN1C and that miR-25 could potentially be a therapeutic target for glioma intervention. | ||
| 650 | 7 | |a CDKN1C |2 Elsevier | |
| 650 | 7 | |a UTR |2 Elsevier | |
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| 700 | 1 | |a Gong, Xuhai |4 oth | |
| 700 | 1 | |a Tian, Kaiyu |4 oth | |
| 700 | 1 | |a Chen, Dongkai |4 oth | |
| 700 | 1 | |a Sun, Jiahang |4 oth | |
| 700 | 1 | |a Wang, Guangzhi |4 oth | |
| 700 | 1 | |a Guo, Mian |4 oth | |
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10.1016/j.biopha.2015.02.005 doi GBVA2015014000002.pica (DE-627)ELV029047595 (ELSEVIER)S0753-3322(15)00054-2 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 44.86 bkl Zhang, Jihong verfasserin aut miR-25 promotes glioma cell proliferation by targeting CDKN1C 2015transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier MicroRNAs (miRNA) have oncogenic or tumor-suppressive roles in the development and growth of human glioma. Glioma development is also associated with alteration in the activities and expression of cell cycle regulators, and miRNAs are emerging as important regulators of cell cycle progression. Here, we show that miR-25 is overexpressed in 91% of examined human glioma tissues and 4 out of 6 human glioma cell lines. MiR-25 increases cell proliferation in two independent glioma cell lines. Ectopic expression of miR-25 was found to reduce CDKN1C protein levels by directly targeting its 3′-untranslated region (UTR). Notably, ablation of endogenous miR-25 rescued CDKN1C expression and significantly decreased glioma cell proliferation by facilitating normal cell cycle progression. Our clinical investigation found CDKN1C and miR-25 levels were inversely correlated. Lastly, downregulation of CDKN1 by siRNA blocked the activity of miR-25 on promoting glioma cell proliferation. Overall, our results for the first time show an oncogenic role of miR-25 in human glioma by targeting CDKN1C and that miR-25 could potentially be a therapeutic target for glioma intervention. MicroRNAs (miRNA) have oncogenic or tumor-suppressive roles in the development and growth of human glioma. Glioma development is also associated with alteration in the activities and expression of cell cycle regulators, and miRNAs are emerging as important regulators of cell cycle progression. Here, we show that miR-25 is overexpressed in 91% of examined human glioma tissues and 4 out of 6 human glioma cell lines. MiR-25 increases cell proliferation in two independent glioma cell lines. Ectopic expression of miR-25 was found to reduce CDKN1C protein levels by directly targeting its 3′-untranslated region (UTR). Notably, ablation of endogenous miR-25 rescued CDKN1C expression and significantly decreased glioma cell proliferation by facilitating normal cell cycle progression. Our clinical investigation found CDKN1C and miR-25 levels were inversely correlated. Lastly, downregulation of CDKN1 by siRNA blocked the activity of miR-25 on promoting glioma cell proliferation. Overall, our results for the first time show an oncogenic role of miR-25 in human glioma by targeting CDKN1C and that miR-25 could potentially be a therapeutic target for glioma intervention. CDKN1C Elsevier UTR Elsevier NC Elsevier NHA Elsevier microRNA Elsevier Gong, Xuhai oth Tian, Kaiyu oth Chen, Dongkai oth Sun, Jiahang oth Wang, Guangzhi oth Guo, Mian oth Enthalten in Elsevier Science Liao, Gary ELSEVIER A Scoping Review of Registered Clinical Trials of Cellular Therapy for COVID-19 and a 2020 Amsterdam [u.a.] (DE-627)ELV004620771 volume:71 year:2015 pages:7-14 extent:8 https://doi.org/10.1016/j.biopha.2015.02.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.86 Hämatologie VZ AR 71 2015 7-14 8 045F 610 |
| spelling |
10.1016/j.biopha.2015.02.005 doi GBVA2015014000002.pica (DE-627)ELV029047595 (ELSEVIER)S0753-3322(15)00054-2 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 44.86 bkl Zhang, Jihong verfasserin aut miR-25 promotes glioma cell proliferation by targeting CDKN1C 2015transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier MicroRNAs (miRNA) have oncogenic or tumor-suppressive roles in the development and growth of human glioma. Glioma development is also associated with alteration in the activities and expression of cell cycle regulators, and miRNAs are emerging as important regulators of cell cycle progression. Here, we show that miR-25 is overexpressed in 91% of examined human glioma tissues and 4 out of 6 human glioma cell lines. MiR-25 increases cell proliferation in two independent glioma cell lines. Ectopic expression of miR-25 was found to reduce CDKN1C protein levels by directly targeting its 3′-untranslated region (UTR). Notably, ablation of endogenous miR-25 rescued CDKN1C expression and significantly decreased glioma cell proliferation by facilitating normal cell cycle progression. Our clinical investigation found CDKN1C and miR-25 levels were inversely correlated. Lastly, downregulation of CDKN1 by siRNA blocked the activity of miR-25 on promoting glioma cell proliferation. Overall, our results for the first time show an oncogenic role of miR-25 in human glioma by targeting CDKN1C and that miR-25 could potentially be a therapeutic target for glioma intervention. MicroRNAs (miRNA) have oncogenic or tumor-suppressive roles in the development and growth of human glioma. Glioma development is also associated with alteration in the activities and expression of cell cycle regulators, and miRNAs are emerging as important regulators of cell cycle progression. Here, we show that miR-25 is overexpressed in 91% of examined human glioma tissues and 4 out of 6 human glioma cell lines. MiR-25 increases cell proliferation in two independent glioma cell lines. Ectopic expression of miR-25 was found to reduce CDKN1C protein levels by directly targeting its 3′-untranslated region (UTR). Notably, ablation of endogenous miR-25 rescued CDKN1C expression and significantly decreased glioma cell proliferation by facilitating normal cell cycle progression. Our clinical investigation found CDKN1C and miR-25 levels were inversely correlated. Lastly, downregulation of CDKN1 by siRNA blocked the activity of miR-25 on promoting glioma cell proliferation. Overall, our results for the first time show an oncogenic role of miR-25 in human glioma by targeting CDKN1C and that miR-25 could potentially be a therapeutic target for glioma intervention. CDKN1C Elsevier UTR Elsevier NC Elsevier NHA Elsevier microRNA Elsevier Gong, Xuhai oth Tian, Kaiyu oth Chen, Dongkai oth Sun, Jiahang oth Wang, Guangzhi oth Guo, Mian oth Enthalten in Elsevier Science Liao, Gary ELSEVIER A Scoping Review of Registered Clinical Trials of Cellular Therapy for COVID-19 and a 2020 Amsterdam [u.a.] (DE-627)ELV004620771 volume:71 year:2015 pages:7-14 extent:8 https://doi.org/10.1016/j.biopha.2015.02.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.86 Hämatologie VZ AR 71 2015 7-14 8 045F 610 |
| allfields_unstemmed |
10.1016/j.biopha.2015.02.005 doi GBVA2015014000002.pica (DE-627)ELV029047595 (ELSEVIER)S0753-3322(15)00054-2 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 44.86 bkl Zhang, Jihong verfasserin aut miR-25 promotes glioma cell proliferation by targeting CDKN1C 2015transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier MicroRNAs (miRNA) have oncogenic or tumor-suppressive roles in the development and growth of human glioma. Glioma development is also associated with alteration in the activities and expression of cell cycle regulators, and miRNAs are emerging as important regulators of cell cycle progression. Here, we show that miR-25 is overexpressed in 91% of examined human glioma tissues and 4 out of 6 human glioma cell lines. MiR-25 increases cell proliferation in two independent glioma cell lines. Ectopic expression of miR-25 was found to reduce CDKN1C protein levels by directly targeting its 3′-untranslated region (UTR). Notably, ablation of endogenous miR-25 rescued CDKN1C expression and significantly decreased glioma cell proliferation by facilitating normal cell cycle progression. Our clinical investigation found CDKN1C and miR-25 levels were inversely correlated. Lastly, downregulation of CDKN1 by siRNA blocked the activity of miR-25 on promoting glioma cell proliferation. Overall, our results for the first time show an oncogenic role of miR-25 in human glioma by targeting CDKN1C and that miR-25 could potentially be a therapeutic target for glioma intervention. MicroRNAs (miRNA) have oncogenic or tumor-suppressive roles in the development and growth of human glioma. Glioma development is also associated with alteration in the activities and expression of cell cycle regulators, and miRNAs are emerging as important regulators of cell cycle progression. Here, we show that miR-25 is overexpressed in 91% of examined human glioma tissues and 4 out of 6 human glioma cell lines. MiR-25 increases cell proliferation in two independent glioma cell lines. Ectopic expression of miR-25 was found to reduce CDKN1C protein levels by directly targeting its 3′-untranslated region (UTR). Notably, ablation of endogenous miR-25 rescued CDKN1C expression and significantly decreased glioma cell proliferation by facilitating normal cell cycle progression. Our clinical investigation found CDKN1C and miR-25 levels were inversely correlated. Lastly, downregulation of CDKN1 by siRNA blocked the activity of miR-25 on promoting glioma cell proliferation. Overall, our results for the first time show an oncogenic role of miR-25 in human glioma by targeting CDKN1C and that miR-25 could potentially be a therapeutic target for glioma intervention. CDKN1C Elsevier UTR Elsevier NC Elsevier NHA Elsevier microRNA Elsevier Gong, Xuhai oth Tian, Kaiyu oth Chen, Dongkai oth Sun, Jiahang oth Wang, Guangzhi oth Guo, Mian oth Enthalten in Elsevier Science Liao, Gary ELSEVIER A Scoping Review of Registered Clinical Trials of Cellular Therapy for COVID-19 and a 2020 Amsterdam [u.a.] (DE-627)ELV004620771 volume:71 year:2015 pages:7-14 extent:8 https://doi.org/10.1016/j.biopha.2015.02.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.86 Hämatologie VZ AR 71 2015 7-14 8 045F 610 |
| allfieldsGer |
10.1016/j.biopha.2015.02.005 doi GBVA2015014000002.pica (DE-627)ELV029047595 (ELSEVIER)S0753-3322(15)00054-2 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 44.86 bkl Zhang, Jihong verfasserin aut miR-25 promotes glioma cell proliferation by targeting CDKN1C 2015transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier MicroRNAs (miRNA) have oncogenic or tumor-suppressive roles in the development and growth of human glioma. Glioma development is also associated with alteration in the activities and expression of cell cycle regulators, and miRNAs are emerging as important regulators of cell cycle progression. Here, we show that miR-25 is overexpressed in 91% of examined human glioma tissues and 4 out of 6 human glioma cell lines. MiR-25 increases cell proliferation in two independent glioma cell lines. Ectopic expression of miR-25 was found to reduce CDKN1C protein levels by directly targeting its 3′-untranslated region (UTR). Notably, ablation of endogenous miR-25 rescued CDKN1C expression and significantly decreased glioma cell proliferation by facilitating normal cell cycle progression. Our clinical investigation found CDKN1C and miR-25 levels were inversely correlated. Lastly, downregulation of CDKN1 by siRNA blocked the activity of miR-25 on promoting glioma cell proliferation. Overall, our results for the first time show an oncogenic role of miR-25 in human glioma by targeting CDKN1C and that miR-25 could potentially be a therapeutic target for glioma intervention. MicroRNAs (miRNA) have oncogenic or tumor-suppressive roles in the development and growth of human glioma. Glioma development is also associated with alteration in the activities and expression of cell cycle regulators, and miRNAs are emerging as important regulators of cell cycle progression. Here, we show that miR-25 is overexpressed in 91% of examined human glioma tissues and 4 out of 6 human glioma cell lines. MiR-25 increases cell proliferation in two independent glioma cell lines. Ectopic expression of miR-25 was found to reduce CDKN1C protein levels by directly targeting its 3′-untranslated region (UTR). Notably, ablation of endogenous miR-25 rescued CDKN1C expression and significantly decreased glioma cell proliferation by facilitating normal cell cycle progression. Our clinical investigation found CDKN1C and miR-25 levels were inversely correlated. Lastly, downregulation of CDKN1 by siRNA blocked the activity of miR-25 on promoting glioma cell proliferation. Overall, our results for the first time show an oncogenic role of miR-25 in human glioma by targeting CDKN1C and that miR-25 could potentially be a therapeutic target for glioma intervention. CDKN1C Elsevier UTR Elsevier NC Elsevier NHA Elsevier microRNA Elsevier Gong, Xuhai oth Tian, Kaiyu oth Chen, Dongkai oth Sun, Jiahang oth Wang, Guangzhi oth Guo, Mian oth Enthalten in Elsevier Science Liao, Gary ELSEVIER A Scoping Review of Registered Clinical Trials of Cellular Therapy for COVID-19 and a 2020 Amsterdam [u.a.] (DE-627)ELV004620771 volume:71 year:2015 pages:7-14 extent:8 https://doi.org/10.1016/j.biopha.2015.02.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.86 Hämatologie VZ AR 71 2015 7-14 8 045F 610 |
| allfieldsSound |
10.1016/j.biopha.2015.02.005 doi GBVA2015014000002.pica (DE-627)ELV029047595 (ELSEVIER)S0753-3322(15)00054-2 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 44.86 bkl Zhang, Jihong verfasserin aut miR-25 promotes glioma cell proliferation by targeting CDKN1C 2015transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier MicroRNAs (miRNA) have oncogenic or tumor-suppressive roles in the development and growth of human glioma. Glioma development is also associated with alteration in the activities and expression of cell cycle regulators, and miRNAs are emerging as important regulators of cell cycle progression. Here, we show that miR-25 is overexpressed in 91% of examined human glioma tissues and 4 out of 6 human glioma cell lines. MiR-25 increases cell proliferation in two independent glioma cell lines. Ectopic expression of miR-25 was found to reduce CDKN1C protein levels by directly targeting its 3′-untranslated region (UTR). Notably, ablation of endogenous miR-25 rescued CDKN1C expression and significantly decreased glioma cell proliferation by facilitating normal cell cycle progression. Our clinical investigation found CDKN1C and miR-25 levels were inversely correlated. Lastly, downregulation of CDKN1 by siRNA blocked the activity of miR-25 on promoting glioma cell proliferation. Overall, our results for the first time show an oncogenic role of miR-25 in human glioma by targeting CDKN1C and that miR-25 could potentially be a therapeutic target for glioma intervention. MicroRNAs (miRNA) have oncogenic or tumor-suppressive roles in the development and growth of human glioma. Glioma development is also associated with alteration in the activities and expression of cell cycle regulators, and miRNAs are emerging as important regulators of cell cycle progression. Here, we show that miR-25 is overexpressed in 91% of examined human glioma tissues and 4 out of 6 human glioma cell lines. MiR-25 increases cell proliferation in two independent glioma cell lines. Ectopic expression of miR-25 was found to reduce CDKN1C protein levels by directly targeting its 3′-untranslated region (UTR). Notably, ablation of endogenous miR-25 rescued CDKN1C expression and significantly decreased glioma cell proliferation by facilitating normal cell cycle progression. Our clinical investigation found CDKN1C and miR-25 levels were inversely correlated. Lastly, downregulation of CDKN1 by siRNA blocked the activity of miR-25 on promoting glioma cell proliferation. Overall, our results for the first time show an oncogenic role of miR-25 in human glioma by targeting CDKN1C and that miR-25 could potentially be a therapeutic target for glioma intervention. CDKN1C Elsevier UTR Elsevier NC Elsevier NHA Elsevier microRNA Elsevier Gong, Xuhai oth Tian, Kaiyu oth Chen, Dongkai oth Sun, Jiahang oth Wang, Guangzhi oth Guo, Mian oth Enthalten in Elsevier Science Liao, Gary ELSEVIER A Scoping Review of Registered Clinical Trials of Cellular Therapy for COVID-19 and a 2020 Amsterdam [u.a.] (DE-627)ELV004620771 volume:71 year:2015 pages:7-14 extent:8 https://doi.org/10.1016/j.biopha.2015.02.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.86 Hämatologie VZ AR 71 2015 7-14 8 045F 610 |
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mir-25 promotes glioma cell proliferation by targeting cdkn1c |
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miR-25 promotes glioma cell proliferation by targeting CDKN1C |
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MicroRNAs (miRNA) have oncogenic or tumor-suppressive roles in the development and growth of human glioma. Glioma development is also associated with alteration in the activities and expression of cell cycle regulators, and miRNAs are emerging as important regulators of cell cycle progression. Here, we show that miR-25 is overexpressed in 91% of examined human glioma tissues and 4 out of 6 human glioma cell lines. MiR-25 increases cell proliferation in two independent glioma cell lines. Ectopic expression of miR-25 was found to reduce CDKN1C protein levels by directly targeting its 3′-untranslated region (UTR). Notably, ablation of endogenous miR-25 rescued CDKN1C expression and significantly decreased glioma cell proliferation by facilitating normal cell cycle progression. Our clinical investigation found CDKN1C and miR-25 levels were inversely correlated. Lastly, downregulation of CDKN1 by siRNA blocked the activity of miR-25 on promoting glioma cell proliferation. Overall, our results for the first time show an oncogenic role of miR-25 in human glioma by targeting CDKN1C and that miR-25 could potentially be a therapeutic target for glioma intervention. |
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MicroRNAs (miRNA) have oncogenic or tumor-suppressive roles in the development and growth of human glioma. Glioma development is also associated with alteration in the activities and expression of cell cycle regulators, and miRNAs are emerging as important regulators of cell cycle progression. Here, we show that miR-25 is overexpressed in 91% of examined human glioma tissues and 4 out of 6 human glioma cell lines. MiR-25 increases cell proliferation in two independent glioma cell lines. Ectopic expression of miR-25 was found to reduce CDKN1C protein levels by directly targeting its 3′-untranslated region (UTR). Notably, ablation of endogenous miR-25 rescued CDKN1C expression and significantly decreased glioma cell proliferation by facilitating normal cell cycle progression. Our clinical investigation found CDKN1C and miR-25 levels were inversely correlated. Lastly, downregulation of CDKN1 by siRNA blocked the activity of miR-25 on promoting glioma cell proliferation. Overall, our results for the first time show an oncogenic role of miR-25 in human glioma by targeting CDKN1C and that miR-25 could potentially be a therapeutic target for glioma intervention. |
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MicroRNAs (miRNA) have oncogenic or tumor-suppressive roles in the development and growth of human glioma. Glioma development is also associated with alteration in the activities and expression of cell cycle regulators, and miRNAs are emerging as important regulators of cell cycle progression. Here, we show that miR-25 is overexpressed in 91% of examined human glioma tissues and 4 out of 6 human glioma cell lines. MiR-25 increases cell proliferation in two independent glioma cell lines. Ectopic expression of miR-25 was found to reduce CDKN1C protein levels by directly targeting its 3′-untranslated region (UTR). Notably, ablation of endogenous miR-25 rescued CDKN1C expression and significantly decreased glioma cell proliferation by facilitating normal cell cycle progression. Our clinical investigation found CDKN1C and miR-25 levels were inversely correlated. Lastly, downregulation of CDKN1 by siRNA blocked the activity of miR-25 on promoting glioma cell proliferation. Overall, our results for the first time show an oncogenic role of miR-25 in human glioma by targeting CDKN1C and that miR-25 could potentially be a therapeutic target for glioma intervention. |
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