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.
A new preprint design is coming!
We have improved readability, clarity, accessibility, and opportunities for engagement.
Research
Ruirong Xu
Shandong University of Traditional Chinese Medicine Affiliated Hospital
Corresponding Author
ORCiD: https://orcid.org/0000-0002-9871-1542
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Objective
This study aims to explore the role and mechanism of Cdc20 on Ara-c chemosensitivity of AML cells.
Methods
Evaluation experiments of effects of Cdc20 on Ara-c chemosensitivity were performed with AML cell transfected with constructs overexpressing Cdc20 or AML cell transfected with Cdc20 shRNA through observing cell viability, apoptosis rate,expression of apoptosis protein.The level of autophagy was assessed by transmission electron microscopy and western blotting.
Results
After exposure to Ara-c, Cdc20 expression is down-regulated. Intracellular Cdc20 expression inhibited Ara-c-induced apoptosis as shown by increasing cell viability and decreasing expression of cleaved caspase3.The expression of LC3B was mediated by Cdc20 expression,which further inhibits autophagy. Moreover, Cdc20 mediated LC3B-decreasing promotes the expression of P-Akt and P-ERK and inhibits ROS generation.
Conclusion
It was determined that Cdc20 promoted the degradation of LC3B, thereby inhibiting autophagy and decreasing Ara-c-induced apoptosis in AML cells.
Keywords
Acute myelogenous leukemia, apoptosis, Cdc20, LC3B
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Figure 7
Loading...
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 12 Feb, 2021
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Cell Communication and Signaling
Learn more about our company.
A new preprint design is coming!
We have improved readability, clarity, accessibility, and opportunities for engagement.
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
Ruirong Xu
Shandong University of Traditional Chinese Medicine Affiliated Hospital
Corresponding Author
ORCiD: https://orcid.org/0000-0002-9871-1542
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 12 Feb, 2021
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Cell Communication and Signaling
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Objective
This study aims to explore the role and mechanism of Cdc20 on Ara-c chemosensitivity of AML cells.
Methods
Evaluation experiments of effects of Cdc20 on Ara-c chemosensitivity were performed with AML cell transfected with constructs overexpressing Cdc20 or AML cell transfected with Cdc20 shRNA through observing cell viability, apoptosis rate,expression of apoptosis protein.The level of autophagy was assessed by transmission electron microscopy and western blotting.
Results
After exposure to Ara-c, Cdc20 expression is down-regulated. Intracellular Cdc20 expression inhibited Ara-c-induced apoptosis as shown by increasing cell viability and decreasing expression of cleaved caspase3.The expression of LC3B was mediated by Cdc20 expression,which further inhibits autophagy. Moreover, Cdc20 mediated LC3B-decreasing promotes the expression of P-Akt and P-ERK and inhibits ROS generation.
Conclusion
It was determined that Cdc20 promoted the degradation of LC3B, thereby inhibiting autophagy and decreasing Ara-c-induced apoptosis in AML cells.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Figure 7
Loading...