This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Research
Chuize Kong
First Affiliated Hospital of China Medical University
Corresponding Author
ORCiD: https://orcid.org/0000-0002-0875-2173
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This work is licensed under a CC BY 4.0 License. Read Full License
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.
Keywords
MicroRNA, renal cell carcinoma, DAPK1, STAT3, apoptosis
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This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Research
Chuize Kong
First Affiliated Hospital of China Medical University
Corresponding Author
ORCiD: https://orcid.org/0000-0002-0875-2173
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
View the published article at Cancer Gene Therapy.
Version 1
Posted 16 Apr, 2020
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
License:
This work is licensed under a CC BY 4.0 License. Read Full License
View the published article at Cancer Gene Therapy.
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
The full text of this article is available to read as a PDF.
This is a list of supplementary files associated with this preprint. Click to download.
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