Review for "Old Mice Have Less Transcriptional Activation but Similar Periosteal Cell Proliferation Compared to Young‐Adult Mice in Response to In Vivo Mechanical Loading"

2020 ◽  
Author(s):  
Bettina M Willie
Keyword(s):  
Cell Proliferation ◽  
Young Adult ◽  
Mechanical Loading ◽  
Transcriptional Activation ◽  
Periosteal Cell ◽  
Old Mice

scholarly journals Old Mice Have Less Transcriptional Activation But Similar Periosteal Cell Proliferation Compared to Young‐Adult Mice in Response to in vivo Mechanical Loading

2020 ◽  
Vol 35 (9) ◽  
pp. 1751-1764 ◽  
Author(s):  
Christopher J Chermside‐Scabbo ◽  
Taylor L Harris ◽  
Michael D Brodt ◽  
Ingrid Braenne ◽  
Bo Zhang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Young Adult ◽  
Mechanical Loading ◽  
Transcriptional Activation ◽  
Adult Mice ◽  
Periosteal Cell ◽  
Old Mice

Author response for "Old Mice Have Less Transcriptional Activation but Similar Periosteal Cell Proliferation Compared to Young‐Adult Mice in Response to In Vivo Mechanical Loading"

2020 ◽  
Author(s):  
Christopher J Chermside‐Scabbo ◽  
Taylor L Harris ◽  
Michael D Brodt ◽  
Ingrid Braenne ◽  
Bo Zhang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Young Adult ◽  
Mechanical Loading ◽  
Transcriptional Activation ◽  
Author Response ◽  
Periosteal Cell ◽  
Old Mice

Author response for "Old Mice Have Less Transcriptional Activation but Similar Periosteal Cell Proliferation Compared to Young‐Adult Mice in Response to In Vivo Mechanical Loading"

2020 ◽  
Author(s):  
Christopher J Chermside‐Scabbo ◽  
Taylor L Harris ◽  
Michael D Brodt ◽  
Ingrid Braenne ◽  
Bo Zhang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Young Adult ◽  
Mechanical Loading ◽  
Transcriptional Activation ◽  
Author Response ◽  
Periosteal Cell ◽  
Old Mice

scholarly journals CDK13 upregulation-induced formation of the positive feedback loop among circCDK13, miR-212-5p/miR-449a and E2F5 contributes to prostate carcinogenesis

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Jin-Chun Qi ◽  
Zhan Yang ◽  
Tao Lin ◽  
Long Ma ◽  
Ya-Xuan Wang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Transcriptional Activation ◽  
Positive Feedback ◽  
Feedback Loop ◽  
Biological Effects ◽  
Therapeutic Benefit ◽  
Loss Of Function ◽  
Positive Feedback Loop

Abstract Background Both E2F transcription factor and cyclin-dependent kinases (CDKs), which increase or decrease E2F activity by phosphorylating E2F or its partner, are involved in the control of cell proliferation, and some circRNAs and miRNAs regulate the expression of E2F and CDKs. However, little is known about whether dysregulation among E2Fs, CDKs, circRNAs and miRNAs occurs in human PCa. Methods The expression levels of CDK13 in PCa tissues and different cell lines were determined by quantitative real-time PCR and Western blot analysis. In vitro and in vivo assays were preformed to explore the biological effects of CDK13 in PCa cells. Co-immunoprecipitation anlysis coupled with mass spectrometry was used to identify E2F5 interaction with CDK13. A CRISPR-Cas9 complex was used to activate endogenous CDK13 and circCDK13 expression. Furthermore, the mechanism of circCDK13 was investigated by using loss-of-function and gain-of-function assays in vitro and in vivo. Results Here we show that CDK13 is significantly upregulated in human PCa tissues. CDK13 depletion and overexpression in PCa cells decrease and increase, respectively, cell proliferation, and the pro-proliferation effect of CDK13 is strengthened by its interaction with E2F5. Mechanistically, transcriptional activation of endogenous CDK13, but not the forced expression of CDK13 by its expression vector, remarkably promotes E2F5 protein expression by facilitating circCDK13 formation. Further, the upregulation of E2F5 enhances CDK13 transcription and promotes circCDK13 biogenesis, which in turn sponges miR-212-5p/449a and thus relieves their repression of the E2F5 expression, subsequently leading to the upregulation of E2F5 expression and PCa cell proliferation. Conclusions These findings suggest that CDK13 upregulation-induced formation of the positive feedback loop among circCDK13, miR-212-5p/miR-449a and E2F5 is responsible for PCa development. Targeting this newly identified regulatory axis may provide therapeutic benefit against PCa progression and drug resistance.

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