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Background: Mounting evidence has shown that Circular RNAs (circRNAs) are associated with initiation and progression of human cancers. However, the expression and function of circRNAs in the development of osteosarcoma (OS) remain unclear.
Methods: In this study, the expression profiles of circRNA circ-ANKS1B in OS were identified through qRT-PCR and in situ hybridization (ISH). The relationships between expression of circ-ANKS1B and clinicopathological features of OS patients was analyzed. Cell proliferation potential, migration and invasion ability of OS cells were evaluated through CCK8, colony formation, transwell and wound healing assays in vitro. Xenograft nude mouse experiment was performed to investigate tumor formation ability in vivo. The downstream regulated microRNA of circ-ANKS1B was proved via qRT-PCR and dual-luciferase reporter.
Results: We found expression of circ-ANKS1B was markedly overexpressed in OS cell lines and tumor tissues, and high expression of circ-ANKS1B was correlated with advanced TNM stage and poor prognosis of OS patients. The results of functional experiments showed that depletion of circ-ANKS1B could inhibit proliferation and invasion ability of OS cells in vitro, and tumor formation ability in vivo. Further mechanistic studies revealed that circ-ANKS1B could sponge endogenous miR-149-5p and partially reversed the suppressive effect of miR-149-5p in OS cells. Furthermore, we demonstrated that circ-ANKS1B regulated Ki-67 expression by sponging miR-149-5p. Conclusions: In summary, our data showed that circ-ANKS1B accelerated cell growth and invasion in OS by sponging miR-149-5p and regulating Ki-67.
Keywords
circ-ANKS1B, miR-149, progression, osteosarcoma, Ki-67
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On 03 Apr, 2020
Reviewer #1 agreed
On 17 Feb, 2020
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On 12 Feb, 2020
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This preprint is under consideration at Cancer Cell International. A preprint is 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.
Learn more about In Review
Primary research
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Under Revision
Version 2
Posted 13 Feb, 2020
No community comments so far
Editorial decision: Minor revision
On 13 Apr, 2020
Review #1 received
Received 10 Apr, 2020
Review #2 received
Received 10 Apr, 2020
Reviewer #3 agreed
On 06 Apr, 2020
Review #3 received
Received 06 Apr, 2020
Reviewer #2 agreed
On 03 Apr, 2020
Reviewer #1 agreed
On 17 Feb, 2020
Editor assigned
On 13 Feb, 2020
Reviewers invited
Invitations sent on 13 Feb, 2020
Submission checks complete
On 12 Feb, 2020
Editor invited
On 12 Feb, 2020
No comments provided
Editorial decision: Revise Before Review
On 09 Feb, 2020
Editor assigned
On 06 Feb, 2020
Editor invited
On 05 Feb, 2020
Submission checks complete
On 03 Feb, 2020
First submitted
On 01 Feb, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Cancer Biology
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: Mounting evidence has shown that Circular RNAs (circRNAs) are associated with initiation and progression of human cancers. However, the expression and function of circRNAs in the development of osteosarcoma (OS) remain unclear.
Methods: In this study, the expression profiles of circRNA circ-ANKS1B in OS were identified through qRT-PCR and in situ hybridization (ISH). The relationships between expression of circ-ANKS1B and clinicopathological features of OS patients was analyzed. Cell proliferation potential, migration and invasion ability of OS cells were evaluated through CCK8, colony formation, transwell and wound healing assays in vitro. Xenograft nude mouse experiment was performed to investigate tumor formation ability in vivo. The downstream regulated microRNA of circ-ANKS1B was proved via qRT-PCR and dual-luciferase reporter.
Results: We found expression of circ-ANKS1B was markedly overexpressed in OS cell lines and tumor tissues, and high expression of circ-ANKS1B was correlated with advanced TNM stage and poor prognosis of OS patients. The results of functional experiments showed that depletion of circ-ANKS1B could inhibit proliferation and invasion ability of OS cells in vitro, and tumor formation ability in vivo. Further mechanistic studies revealed that circ-ANKS1B could sponge endogenous miR-149-5p and partially reversed the suppressive effect of miR-149-5p in OS cells. Furthermore, we demonstrated that circ-ANKS1B regulated Ki-67 expression by sponging miR-149-5p. Conclusions: In summary, our data showed that circ-ANKS1B accelerated cell growth and invasion in OS by sponging miR-149-5p and regulating Ki-67.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Figure 7
Figure 8
This is a list of supplementary files associated with this preprint. Click to download.
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