See the published version of this preprint at Journal of Ovarian Research.
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
Research
Yan Wang
First Affiliated Hospital of Harbin Medical University
Corresponding Author
ORCiD: https://orcid.org/0000-0003-4999-4926
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: Ovarian cancer (OC) is a major cause of death among women due to the lack of early screening methods and its complex pathological progression. Increasing evidence has indicated that microRNAs regulate gene expression in tumours by interacting with mRNAs. Although the research regarding OC and microRNAs is extensive, the vital role of MIR502 in OC remains unclear.
Methods: We integrated two microRNA expression arrays from GEO to identify differentially expressed genes. The Kaplan–Meier method was used to screen for miRNAs that had an influence on survival outcome. Upstream regulators of MIR502 were predicted by JASPAR and verified by ChIP-seq data. The LinkedOmics database was used to study genes that were correlated with MIR502. Gene Set Enrichment Analysis (GSEA) was conducted for functional annotation with GO and KEGG pathway enrichment analyses by using the open access WebGestalt tool. We constructed a PPI network by using STRING to further explore the core proteins.
Results: We found that the expression level of MIR502 was significantly downregulated in OC, which was related to poor overall survival. NRF1, as an upstream regulator of MIR502, was predicted by JASPAR and verified by ChIP-seq data. In addition, anti-apoptosis and pro-proliferation genes in the Hippo signalling pathway, including CCND1, MYC, FGF1 and GLI2, were negatively regulated by MIR502, as shown in the GO and KEGG pathway enrichment results. The PPI network further demonstrated that CCND1 and MYCN were at core positions in the development of ovarian cancer.
Conclusions: MIR502, which is regulated by NRF1, acts as a tumour suppressor gene to accelerate apoptosis and suppress proliferation by targeting the Hippo signalling pathway in ovarian cancer.
Keywords
MIR502, NRF1, Hippo signaling pathway, ovarian cancer
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Figure 7
Figure 8
Figure 9
Figure 10
Loading...
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 Journal of Ovarian Research.
Version 2
Posted 23 Jun, 2020
No community comments so far
Reviewer #1 agreed
On 23 Jun, 2020
Review #1 received
Received 23 Jun, 2020
Editorial decision: Accept
On 23 Jun, 2020
Editor assigned
On 22 Jun, 2020
Reviewers invited
Invitations sent on 22 Jun, 2020
Submission checks complete
On 21 Jun, 2020
Editor invited
On 21 Jun, 2020
No comments provided
Review #1 received
Received 08 Jun, 2020
Editorial decision: Major revision
On 08 Jun, 2020
Reviewer #1 agreed
On 28 May, 2020
Reviewers invited
Invitations sent on 16 May, 2020
Editor assigned
On 11 May, 2020
Submission checks complete
On 10 May, 2020
Editor invited
On 10 May, 2020
First submitted
On 08 May, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Learn more about our company.
See the published version of this preprint at Journal of Ovarian Research.
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
Research
Yan Wang
First Affiliated Hospital of Harbin Medical University
Corresponding Author
ORCiD: https://orcid.org/0000-0003-4999-4926
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 Journal of Ovarian Research.
Version 2
Posted 23 Jun, 2020
No community comments so far
Reviewer #1 agreed
On 23 Jun, 2020
Review #1 received
Received 23 Jun, 2020
Editorial decision: Accept
On 23 Jun, 2020
Editor assigned
On 22 Jun, 2020
Reviewers invited
Invitations sent on 22 Jun, 2020
Submission checks complete
On 21 Jun, 2020
Editor invited
On 21 Jun, 2020
No comments provided
Review #1 received
Received 08 Jun, 2020
Editorial decision: Major revision
On 08 Jun, 2020
Reviewer #1 agreed
On 28 May, 2020
Reviewers invited
Invitations sent on 16 May, 2020
Editor assigned
On 11 May, 2020
Submission checks complete
On 10 May, 2020
Editor invited
On 10 May, 2020
First submitted
On 08 May, 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 Journal of Ovarian Research.
Background: Ovarian cancer (OC) is a major cause of death among women due to the lack of early screening methods and its complex pathological progression. Increasing evidence has indicated that microRNAs regulate gene expression in tumours by interacting with mRNAs. Although the research regarding OC and microRNAs is extensive, the vital role of MIR502 in OC remains unclear.
Methods: We integrated two microRNA expression arrays from GEO to identify differentially expressed genes. The Kaplan–Meier method was used to screen for miRNAs that had an influence on survival outcome. Upstream regulators of MIR502 were predicted by JASPAR and verified by ChIP-seq data. The LinkedOmics database was used to study genes that were correlated with MIR502. Gene Set Enrichment Analysis (GSEA) was conducted for functional annotation with GO and KEGG pathway enrichment analyses by using the open access WebGestalt tool. We constructed a PPI network by using STRING to further explore the core proteins.
Results: We found that the expression level of MIR502 was significantly downregulated in OC, which was related to poor overall survival. NRF1, as an upstream regulator of MIR502, was predicted by JASPAR and verified by ChIP-seq data. In addition, anti-apoptosis and pro-proliferation genes in the Hippo signalling pathway, including CCND1, MYC, FGF1 and GLI2, were negatively regulated by MIR502, as shown in the GO and KEGG pathway enrichment results. The PPI network further demonstrated that CCND1 and MYCN were at core positions in the development of ovarian cancer.
Conclusions: MIR502, which is regulated by NRF1, acts as a tumour suppressor gene to accelerate apoptosis and suppress proliferation by targeting the Hippo signalling pathway in ovarian cancer.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Figure 7
Figure 8
Figure 9
Figure 10
Loading...