STAT3 regulates miR93-mediated apoptosis through inhibiting DAPK1 in renal cell carcinoma
Signal transducer and activator of transcription 3, STAT3, is an essential member of the STAT family. STAT3 regulates diverse genes mediating inflammatory reaction, cell survival, proliferation, and angiogenesis, and it is aberrantly upregulated and activated in various types of malignancies. Meanwhile, STAT3 signaling is involved in multiple feedback loops and pathways. In this study, we demonstrate that in renal cell carcinoma, miR-93-3p act an oncogenesis role in renal cell carcinoma. It enhanced RCC cell proliferation and suppressed apoptosis. Besides, STAT3 could regulate the transcription of miR-93 by directly binding with its promoter region. miR-93 can inhibit the protein level of death-associated protein kinase 1, DAPK1. What’s more, STAT3 could block the expression of DAPK1 on the level of RNA. Importantly, we verify that, through over-expression, DAPK1 might, in return, suppress the activated-STAT3 entering cell nucleus. Thus, the study uncovers a potential signaling transduction pathway, STAT3-miR93-DAPK1, which is continuously activated, and may provide a novel clinical therapeutic approach for RCC.
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Due to technical limitations, full-text HTML conversion of this manuscript could not be completed. However, the manuscript can be downloaded and accessed as a PDF.
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Posted 16 Apr, 2020
STAT3 regulates miR93-mediated apoptosis through inhibiting DAPK1 in renal cell carcinoma
Posted 16 Apr, 2020
Signal transducer and activator of transcription 3, STAT3, is an essential member of the STAT family. STAT3 regulates diverse genes mediating inflammatory reaction, cell survival, proliferation, and angiogenesis, and it is aberrantly upregulated and activated in various types of malignancies. Meanwhile, STAT3 signaling is involved in multiple feedback loops and pathways. In this study, we demonstrate that in renal cell carcinoma, miR-93-3p act an oncogenesis role in renal cell carcinoma. It enhanced RCC cell proliferation and suppressed apoptosis. Besides, STAT3 could regulate the transcription of miR-93 by directly binding with its promoter region. miR-93 can inhibit the protein level of death-associated protein kinase 1, DAPK1. What’s more, STAT3 could block the expression of DAPK1 on the level of RNA. Importantly, we verify that, through over-expression, DAPK1 might, in return, suppress the activated-STAT3 entering cell nucleus. Thus, the study uncovers a potential signaling transduction pathway, STAT3-miR93-DAPK1, which is continuously activated, and may provide a novel clinical therapeutic approach for RCC.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Due to technical limitations, full-text HTML conversion of this manuscript could not be completed. However, the manuscript can be downloaded and accessed as a PDF.