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Research article
Hong Zhang
Shengjing Hospital of China Medical University
Corresponding Author
ORCiD: https://orcid.org/0000-0003-3327-1328
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background
MicroRNA(miR)-200c has been widely reported to be involved in colon cancer progress. However, the mechanisms of miR-200c in regulating tumor metastasis and growth remain to be fully elucidated. This study aimed to investigate the mechanism of miR-200c targets fucosyltransferase 4 (FUT4) on the proliferation of colon cancer.
Methods
The miR-200c and FUT4 mRNA levels in LoVo and SW480 cells were measured by real-time quantitative polymerase chain reaction. Further, miR-200c mimic, FUT4 siRNA and FUT4 mimic were transfected into cells, separately. Cell counting kit-8, plate colony formation and transwell assays were used to analyse the cells biological behaviour.. Immunofluorescence was used to analyse the Ki-67 expression Moreover, the Wnt/β-catenin pathway-related proteins were detected by western blots. A double luciferase experiment was performed to confirm the relationship between miR-200c and FUT4. In vivo, tumour growth and Wnt/β-catenin pathway-related proteins were also analysed.
Results
In vitro, the expression of miR-200c and FUT4 were negatively correlated in LoVo and SW480 cells (correlation coefficients were -0.9046 and -0.9236, respectively). MiR-200c overexpression inhibited the proliferation, migration and invasion of LoVo and SW480 cells by downregulating FUT4. The Ki67-positive cells and Wnt/β-catenin signalling pathway-related proteins were reduced in the miR-200c overexpression and FUT4 silencing groups. A dual luciferase reporting system identified FUT4 as the target of miR-200c. The results in vivo were further confirmed the foundation of cells study.
Conclusions
In summary, miR-200c overexpression inhibits proliferation of colon cancer targeting FUT4 to downregulate the Wnt/β-catenin pathway, which promises molecular targets to inhibit metastasis for colon cancer therapy.
Keywords
miR-200c, FUT4, colon cancer, Wnt/β-catenin pathway
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.
- blotimages.docx
- SupplementaryFigure1.docx
Supplementary Figure [1]. The original blots of Ki-67, FUT4, β-catenin, Cyclin D1, p-GSK-3β, GSK-3β in Lovo and SW480 cells. (Corresponding to Figure 6 in the manuscript).
- SupplementaryFigure2.docx
Supplementary Figure [2]. The original blots of Ki-67, FUT4, β-catenin, Cyclin D1, p-GSK-3β, GSK-3β in Lovo and SW480 cells. (Corresponding to Figure 8 in the manuscript).
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On 25 Sep, 2020
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Received 23 Sep, 2020
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On 17 Sep, 2020
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On 15 Sep, 2020
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Received 15 Sep, 2020
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Editor invited
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On 20 Aug, 2020
Review #2 received
Received 17 Aug, 2020
Reviewer #2 agreed
On 29 Jul, 2020
Reviewer #3 agreed
On 29 Jul, 2020
Review #1 received
Received 24 Jun, 2020
Reviewer #1 agreed
On 04 Jun, 2020
Editor assigned
On 21 May, 2020
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A new preprint design is coming!
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See the published version of this preprint at BMC Cancer.
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 article
Hong Zhang
Shengjing Hospital of China Medical University
Corresponding Author
ORCiD: https://orcid.org/0000-0003-3327-1328
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 BMC Cancer.
No community comments so far
Submission checks complete
On 21 Nov, 2020
Editorial decision: Accept
On 18 Nov, 2020
Version 4
Posted 13 Nov, 2020
No comments provided
Editor assigned
On 07 Nov, 2020
Submission checks complete
On 07 Nov, 2020
Editor invited
On 07 Nov, 2020
No comments provided
Editorial decision: Minor revision
On 28 Oct, 2020
Editor assigned
On 12 Oct, 2020
Submission checks complete
On 11 Oct, 2020
Editor invited
On 11 Oct, 2020
No comments provided
Editorial decision: Minor revision
On 25 Sep, 2020
Review #2 received
Received 23 Sep, 2020
Reviewer #2 agreed
On 17 Sep, 2020
Reviewer #1 agreed
On 15 Sep, 2020
Review #1 received
Received 15 Sep, 2020
Reviewers invited
Invitations sent on 14 Sep, 2020
Editor assigned
On 08 Sep, 2020
Submission checks complete
On 07 Sep, 2020
Editor invited
On 07 Sep, 2020
No comments provided
Editorial decision: Major revision
On 20 Aug, 2020
Review #2 received
Received 17 Aug, 2020
Reviewer #2 agreed
On 29 Jul, 2020
Reviewer #3 agreed
On 29 Jul, 2020
Review #1 received
Received 24 Jun, 2020
Reviewer #1 agreed
On 04 Jun, 2020
Editor assigned
On 21 May, 2020
Reviewers invited
Invitations sent on 21 May, 2020
Submission checks complete
On 20 May, 2020
Editor invited
On 14 May, 2020
First submitted
On 06 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 BMC Cancer.
Background
MicroRNA(miR)-200c has been widely reported to be involved in colon cancer progress. However, the mechanisms of miR-200c in regulating tumor metastasis and growth remain to be fully elucidated. This study aimed to investigate the mechanism of miR-200c targets fucosyltransferase 4 (FUT4) on the proliferation of colon cancer.
Methods
The miR-200c and FUT4 mRNA levels in LoVo and SW480 cells were measured by real-time quantitative polymerase chain reaction. Further, miR-200c mimic, FUT4 siRNA and FUT4 mimic were transfected into cells, separately. Cell counting kit-8, plate colony formation and transwell assays were used to analyse the cells biological behaviour.. Immunofluorescence was used to analyse the Ki-67 expression Moreover, the Wnt/β-catenin pathway-related proteins were detected by western blots. A double luciferase experiment was performed to confirm the relationship between miR-200c and FUT4. In vivo, tumour growth and Wnt/β-catenin pathway-related proteins were also analysed.
Results
In vitro, the expression of miR-200c and FUT4 were negatively correlated in LoVo and SW480 cells (correlation coefficients were -0.9046 and -0.9236, respectively). MiR-200c overexpression inhibited the proliferation, migration and invasion of LoVo and SW480 cells by downregulating FUT4. The Ki67-positive cells and Wnt/β-catenin signalling pathway-related proteins were reduced in the miR-200c overexpression and FUT4 silencing groups. A dual luciferase reporting system identified FUT4 as the target of miR-200c. The results in vivo were further confirmed the foundation of cells study.
Conclusions
In summary, miR-200c overexpression inhibits proliferation of colon cancer targeting FUT4 to downregulate the Wnt/β-catenin pathway, which promises molecular targets to inhibit metastasis for colon cancer therapy.
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.
- blotimages.docx
- SupplementaryFigure1.docx
Supplementary Figure [1]. The original blots of Ki-67, FUT4, β-catenin, Cyclin D1, p-GSK-3β, GSK-3β in Lovo and SW480 cells. (Corresponding to Figure 6 in the manuscript).
- SupplementaryFigure2.docx
Supplementary Figure [2]. The original blots of Ki-67, FUT4, β-catenin, Cyclin D1, p-GSK-3β, GSK-3β in Lovo and SW480 cells. (Corresponding to Figure 8 in the manuscript).
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