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circ_0084927 promotes cervical carcinogenesis by sponging miR-1179 that suppresses CDK2, a cell cycle-related gene
Shaohua Liu
Yantai Affiliated Hospital, Binzhou Medical College
Corresponding Author
ORCiD: https://orcid.org/0000-0001-6672-2725
License:
This work is licensed under a CC BY 4.0 License. Read Full License
View the published version at Cancer Cell International.
Background: Cervical cancer (CC) is a highly malignant tumor. found in the lowermost part of the womb. Evolving researchesstudies on CC have unveiled a conceptreported that circRNA exerts important rolesplays a crucial role in CC progression. In this study, we mainly exploredinvestigated the rolemain function of a novel circRNA, circ_0084927, and its regulatory network in theCC development of CC.
Methods: qRT-PCR was applied to evaluate the expression of circ_0084927, miR-1179, and CDK2 mRNA in CC tissues and cells. Dual-luciferase reporting experiments and RNA immunoprecipitation (RIP) assay were conducted to validate the target relationship of miR-1179 with circ_0084927 and CDK2 mRNA. CCK-8 and BrdU assay wasassays were also used to evaluate CC cell proliferation. The adhesion and apoptosis phenotypes of CC cells were measured byusing cell-matrix adhesion and caspase 3 activation assay. Flow cytometry was also employed to detect the CC cell cycle.
Results: Our results indicated that circ_0084927 was up-regulated in CC tissues and cells, and. Findings also revealed that circ_0084927 silence inhibited CC cell proliferation and adhesion, while facilitating apoptosis as well asand triggering cell cycle arrest. On the other handHowever, miR-1179 down-regulation appeared in CC tissues. Additionally,Apart from observing that circ_0084927 abolished miR-1179’s inhibitory effects on cell proliferation and adhesion. Our study showed, it was found that CDK2 was up-regulated in CC tissues and played awas instrumental in cancer-promoting role. Furthermore, promotion. Also observed was that miR-1179 directly targeted CDK2, thereby inhibiting CDK2’s promotion on the malignant phenotypes of CC cells. Lastly, results indicated that circ_0084927 revoked the inhibitory effect of miR-1179 on CDK2 by sponging miR-1179.
Conclusion: Circcirc_0084927 promoted cervical carcinogenesis by sequestering miR-1179 that, which directly targeted CDK2. Our results shed light onalso provided novel candidate targets for CC treatment in that it revealed the circ_0084927/miR-1179/CDK2 regulatory network that strengthened CC aggressiveness, providing novel candidate targets for CC treatment..
Keywords
cervical cancer, circ_0084927, miR-1179, CDK2
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On 21 Jul, 2020
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On 11 Jul, 2020
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On 10 Jul, 2020
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Editorial decision: Minor revision
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Received 19 Jun, 2020
Review #1 received
Received 15 Jun, 2020
Reviewer #2 agreed
On 10 Jun, 2020
Reviewers invited
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Reviewer #1 agreed
On 08 Jun, 2020
Editor assigned
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Editor invited
On 04 Jun, 2020
No comments provided
Editorial decision: Revise Before Review
On 28 Apr, 2020
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On 27 Apr, 2020
Editor invited
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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
circ_0084927 promotes cervical carcinogenesis by sponging miR-1179 that suppresses CDK2, a cell cycle-related gene
Shaohua Liu
Yantai Affiliated Hospital, Binzhou Medical College
Corresponding Author
ORCiD: https://orcid.org/0000-0001-6672-2725
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
Version 3
Posted 10 Jul, 2020
Published
On 21 Jul, 2020
No community comments so far
Review #1 received
Received 11 Jul, 2020
Editorial decision: Accept
On 11 Jul, 2020
Reviewer #2 agreed
On 11 Jul, 2020
Review #2 received
Received 11 Jul, 2020
Reviewers invited
Invitations sent on 10 Jul, 2020
Reviewer #1 agreed
On 10 Jul, 2020
Editor assigned
On 10 Jul, 2020
Submission checks complete
On 09 Jul, 2020
Editor invited
On 09 Jul, 2020
No comments provided
Editorial decision: Minor revision
On 20 Jun, 2020
Review #2 received
Received 19 Jun, 2020
Review #1 received
Received 15 Jun, 2020
Reviewer #2 agreed
On 10 Jun, 2020
Reviewers invited
Invitations sent on 08 Jun, 2020
Reviewer #1 agreed
On 08 Jun, 2020
Editor assigned
On 05 Jun, 2020
Submission checks complete
On 04 Jun, 2020
Editor invited
On 04 Jun, 2020
No comments provided
Editorial decision: Revise Before Review
On 28 Apr, 2020
Editor assigned
On 27 Apr, 2020
Editor invited
On 26 Apr, 2020
Submission checks complete
On 24 Apr, 2020
First submitted
On 23 Apr, 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
View the published version at Cancer Cell International.
Background: Cervical cancer (CC) is a highly malignant tumor. found in the lowermost part of the womb. Evolving researchesstudies on CC have unveiled a conceptreported that circRNA exerts important rolesplays a crucial role in CC progression. In this study, we mainly exploredinvestigated the rolemain function of a novel circRNA, circ_0084927, and its regulatory network in theCC development of CC.
Methods: qRT-PCR was applied to evaluate the expression of circ_0084927, miR-1179, and CDK2 mRNA in CC tissues and cells. Dual-luciferase reporting experiments and RNA immunoprecipitation (RIP) assay were conducted to validate the target relationship of miR-1179 with circ_0084927 and CDK2 mRNA. CCK-8 and BrdU assay wasassays were also used to evaluate CC cell proliferation. The adhesion and apoptosis phenotypes of CC cells were measured byusing cell-matrix adhesion and caspase 3 activation assay. Flow cytometry was also employed to detect the CC cell cycle.
Results: Our results indicated that circ_0084927 was up-regulated in CC tissues and cells, and. Findings also revealed that circ_0084927 silence inhibited CC cell proliferation and adhesion, while facilitating apoptosis as well asand triggering cell cycle arrest. On the other handHowever, miR-1179 down-regulation appeared in CC tissues. Additionally,Apart from observing that circ_0084927 abolished miR-1179’s inhibitory effects on cell proliferation and adhesion. Our study showed, it was found that CDK2 was up-regulated in CC tissues and played awas instrumental in cancer-promoting role. Furthermore, promotion. Also observed was that miR-1179 directly targeted CDK2, thereby inhibiting CDK2’s promotion on the malignant phenotypes of CC cells. Lastly, results indicated that circ_0084927 revoked the inhibitory effect of miR-1179 on CDK2 by sponging miR-1179.
Conclusion: Circcirc_0084927 promoted cervical carcinogenesis by sequestering miR-1179 that, which directly targeted CDK2. Our results shed light onalso provided novel candidate targets for CC treatment in that it revealed the circ_0084927/miR-1179/CDK2 regulatory network that strengthened CC aggressiveness, providing novel candidate targets for CC treatment..
Figure 1
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