circ_0084927 promotes cervical carcinogenesis by sponging miR-1179 that suppresses CDK2, a cell cycle-related gene
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..
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Posted 10 Jul, 2020
On 21 Jul, 2020
Received 11 Jul, 2020
On 11 Jul, 2020
On 11 Jul, 2020
Received 11 Jul, 2020
Invitations sent on 10 Jul, 2020
On 10 Jul, 2020
On 10 Jul, 2020
On 09 Jul, 2020
On 09 Jul, 2020
On 20 Jun, 2020
Received 19 Jun, 2020
Received 15 Jun, 2020
On 10 Jun, 2020
Invitations sent on 08 Jun, 2020
On 08 Jun, 2020
On 05 Jun, 2020
On 04 Jun, 2020
On 04 Jun, 2020
On 28 Apr, 2020
On 27 Apr, 2020
On 26 Apr, 2020
On 24 Apr, 2020
On 23 Apr, 2020
circ_0084927 promotes cervical carcinogenesis by sponging miR-1179 that suppresses CDK2, a cell cycle-related gene
Posted 10 Jul, 2020
On 21 Jul, 2020
Received 11 Jul, 2020
On 11 Jul, 2020
On 11 Jul, 2020
Received 11 Jul, 2020
Invitations sent on 10 Jul, 2020
On 10 Jul, 2020
On 10 Jul, 2020
On 09 Jul, 2020
On 09 Jul, 2020
On 20 Jun, 2020
Received 19 Jun, 2020
Received 15 Jun, 2020
On 10 Jun, 2020
Invitations sent on 08 Jun, 2020
On 08 Jun, 2020
On 05 Jun, 2020
On 04 Jun, 2020
On 04 Jun, 2020
On 28 Apr, 2020
On 27 Apr, 2020
On 26 Apr, 2020
On 24 Apr, 2020
On 23 Apr, 2020
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
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Figure 7