See the published version of this preprint at Cancer Cell International.
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Primary research
Hui Wang
China-Japan Union Hospital of Jilin University
Corresponding Author
ORCiD: https://orcid.org/0000-0002-1608-3782
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: Long noncoding RNAs (lncRNAs) have recently identified as essential gene modulators in numerous cancers. Previous studies have confirmed the oncogenic role of long intergenic nonprotein-coding RNA 00514 (LINC00514) in some cancers. Nevertheless, its biological function and mechanism remain elusive in triple-negative breast cancer (TNBC).
Methods: Herein, we detected LINC00514 expression level in TNBC tissues and cells via RT-qPCR. The function of LINC00514 in TNBC cellular activities was assessed via colony formation, EdU, wound healing, transwell assays and flow cytometry analysis.
Results: The binding between miR-6504-5p/miR-3139 and LINC00514/CCDC71L was validated by luciferase reporter assay. The data indicated that LINC00514 expression was increased in TNBC tissues and cells. Furthermore, it was manifested that silenced LINC00514 restrained cell proliferative, migratory and invasive abilities and accelerated cell apoptosis. In mechanism, LINC00514 was revealed to sequester miR-6504-5p and miR-3139 in TNBC cells. Furthermore, the low level of miR-6504-5p and miR-3139 was discovered in TNBC tissues and cells. Accordingly, we discovered overexpression of miR-6504-5p or miR-3139 retarded cell growth and migration in TNBC. Later, CCDC71L was recognized as a common downstream gene of miR-6504-5p and miR-3139. Rescue assay verified that overexpressed CCDC71L countervailed the inhibitive influence of LINC00514 knockdown in TNBC cellular process.
Conclusion: MiR-6504-5p and miR-3139 were involved in LINC00514-mediated cellular activities through regulating CCDC71L expression, which provided a novel LINC00514/miR-6504-5p/miR-3139/CCDC71L axis in TNBC.
Keywords
LINC00514, miR-6504-5p, miR-3139, CCDC71L, TNBC
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View the published article at Cancer Cell International.
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Review #3 received
Received 10 Jan, 2021
Editorial decision: Major revision
On 10 Jan, 2021
Reviewer #3 agreed
On 03 Jan, 2021
Reviewer #2 agreed
On 01 Jan, 2021
Review #2 received
Received 01 Jan, 2021
Review #1 received
Received 13 Dec, 2020
Reviewer #1 agreed
On 28 Nov, 2020
Reviewers invited
Invitations sent on 27 Nov, 2020
Editor assigned
On 26 Nov, 2020
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On 26 Nov, 2020
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On 26 Nov, 2020
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On 24 Nov, 2020
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See the published version of this preprint at Cancer Cell International.
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.
Learn more about In Review
Primary research
Hui Wang
China-Japan Union Hospital of Jilin University
Corresponding Author
ORCiD: https://orcid.org/0000-0002-1608-3782
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: Published
View the published article at Cancer Cell International.
Version 1
Posted 04 Dec, 2020
No community comments so far
Review #3 received
Received 10 Jan, 2021
Editorial decision: Major revision
On 10 Jan, 2021
Reviewer #3 agreed
On 03 Jan, 2021
Reviewer #2 agreed
On 01 Jan, 2021
Review #2 received
Received 01 Jan, 2021
Review #1 received
Received 13 Dec, 2020
Reviewer #1 agreed
On 28 Nov, 2020
Reviewers invited
Invitations sent on 27 Nov, 2020
Editor assigned
On 26 Nov, 2020
Submission checks complete
On 26 Nov, 2020
Editor invited
On 26 Nov, 2020
First submitted
On 24 Nov, 2020
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 Cell International.
Background: Long noncoding RNAs (lncRNAs) have recently identified as essential gene modulators in numerous cancers. Previous studies have confirmed the oncogenic role of long intergenic nonprotein-coding RNA 00514 (LINC00514) in some cancers. Nevertheless, its biological function and mechanism remain elusive in triple-negative breast cancer (TNBC).
Methods: Herein, we detected LINC00514 expression level in TNBC tissues and cells via RT-qPCR. The function of LINC00514 in TNBC cellular activities was assessed via colony formation, EdU, wound healing, transwell assays and flow cytometry analysis.
Results: The binding between miR-6504-5p/miR-3139 and LINC00514/CCDC71L was validated by luciferase reporter assay. The data indicated that LINC00514 expression was increased in TNBC tissues and cells. Furthermore, it was manifested that silenced LINC00514 restrained cell proliferative, migratory and invasive abilities and accelerated cell apoptosis. In mechanism, LINC00514 was revealed to sequester miR-6504-5p and miR-3139 in TNBC cells. Furthermore, the low level of miR-6504-5p and miR-3139 was discovered in TNBC tissues and cells. Accordingly, we discovered overexpression of miR-6504-5p or miR-3139 retarded cell growth and migration in TNBC. Later, CCDC71L was recognized as a common downstream gene of miR-6504-5p and miR-3139. Rescue assay verified that overexpressed CCDC71L countervailed the inhibitive influence of LINC00514 knockdown in TNBC cellular process.
Conclusion: MiR-6504-5p and miR-3139 were involved in LINC00514-mediated cellular activities through regulating CCDC71L expression, which provided a novel LINC00514/miR-6504-5p/miR-3139/CCDC71L axis in TNBC.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
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