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Background: Endometrial cancer is one of the most common cancers affecting women's health. The pathogenesis of endometrial cancer involves many signaling pathways which are related with transcription factors or microRNAs. Recent studies have reported that endometrial cancer is also related with the sexual-mediated hormones. The purpose of this research is to treat the endometrial cancer with the hormone-related drugs, and find out the specific molecular mechanism.
Methods: In this study, RL95-2 cells and Ishikawa cells were used as the endometrial cancer cell models. miR-492 was transfected into RL95-2 cells and Ishikawa cells. The miRNA expression was measured by qRT-PCR. The protein expression was measured by western blot. Cell proliferation was monitored using the MTT assay and cell colony formation assay. Cell apoptosis was monitored using EdU assay.
Results: Firstly, the results indicated that metapristone as a kind of hormone-related drugs could significantly inhibit the endometrial cancer cell growth through regulating cell apoptosis-related gene expression. Meanwhile, miR-492 was detected to be highly expressed in the endometrial cancer cell lines. Overexpression of miR-492 could promote the cell proliferation and inhibit the cell apoptosis. Furthermore, the results demonstrated that the downstream target genes of miR-492 were Klf5 and Nrf1, which were inhibited by metapristone. At the animal level, metapristone also inhibited the endometrial cancer cell growth through down-regulating the expression of miR-492 and decreasing the protein level of Klf5 and Nrf1.
Conclusion: Taken together, this study indicated that metapristone inhibited the endometrial cancer cell growth through regulating the cell apoptosis related signaling pathway and the expression of miR-492 and its downstream target genes (Klf5 and Nrf1), which provided the theoretical basis of endometrial cancer in clinical treatment.
Keywords
endometrial cancer, miR-492, metapristone, Klf5, Nrf1
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On 26 Oct, 2020
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Received 26 Oct, 2020
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On 26 Oct, 2020
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On 25 Oct, 2020
Editor invited
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Editorial decision: Major revision
On 07 Jul, 2020
Review #5 received
Received 06 Jul, 2020
Reviewer #7 agreed
On 02 Jul, 2020
Reviewer #6 agreed
On 30 Jun, 2020
Review #3 received
Received 25 Jun, 2020
Reviewer #4 agreed
On 23 Jun, 2020
Reviewer #5 agreed
On 23 Jun, 2020
Review #2 received
Received 23 Jun, 2020
Review #1 received
Received 23 Jun, 2020
Review #4 received
Received 23 Jun, 2020
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On 19 Jun, 2020
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On 18 Jun, 2020
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Reviewer #1 agreed
On 17 Jun, 2020
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On 16 Jun, 2020
Editor invited
On 16 Jun, 2020
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Editor assigned
On 08 Jun, 2020
Editorial decision: Revise Before Review
On 08 Jun, 2020
Submission checks complete
On 07 Jun, 2020
Editor invited
On 07 Jun, 2020
Version 1
Posted 13 Feb, 2020
No comments provided
Editorial decision: Major revision
On 03 Mar, 2020
Review #6 received
Received 02 Mar, 2020
Review #5 received
Received 28 Feb, 2020
Review #3 received
Received 26 Feb, 2020
Review #4 received
Received 26 Feb, 2020
Reviewer #6 agreed
On 17 Feb, 2020
Review #2 received
Received 17 Feb, 2020
Review #1 received
Received 17 Feb, 2020
Reviewer #3 agreed
On 14 Feb, 2020
Reviewer #4 agreed
On 14 Feb, 2020
Reviewer #5 agreed
On 14 Feb, 2020
Reviewers invited
Invitations sent on 14 Feb, 2020
Reviewer #1 agreed
On 14 Feb, 2020
Reviewer #2 agreed
On 14 Feb, 2020
Editor assigned
On 13 Feb, 2020
Editor invited
On 12 Feb, 2020
First submitted
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A new preprint design is coming!
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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
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Complete author information
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Peer Review Timeline
CURRENT STATUS: Published
View the published article at Cancer Cell International.
No community comments so far
Editor assigned
On 25 Nov, 2020
Editorial decision: Accept
On 25 Nov, 2020
Submission checks complete
On 25 Nov, 2020
Editor invited
On 25 Nov, 2020
No comments provided
Editorial decision: Minor revision
On 06 Nov, 2020
Review #3 received
Received 30 Oct, 2020
Review #2 received
Received 30 Oct, 2020
Reviewer #2 agreed
On 26 Oct, 2020
Reviewer #3 agreed
On 26 Oct, 2020
Reviewer #1 agreed
On 26 Oct, 2020
Review #1 received
Received 26 Oct, 2020
Editor assigned
On 26 Oct, 2020
Reviewers invited
Invitations sent on 25 Oct, 2020
Submission checks complete
On 25 Oct, 2020
Editor invited
On 25 Oct, 2020
No comments provided
Editorial decision: Major revision
On 07 Jul, 2020
Review #5 received
Received 06 Jul, 2020
Reviewer #7 agreed
On 02 Jul, 2020
Reviewer #6 agreed
On 30 Jun, 2020
Review #3 received
Received 25 Jun, 2020
Reviewer #4 agreed
On 23 Jun, 2020
Reviewer #5 agreed
On 23 Jun, 2020
Review #2 received
Received 23 Jun, 2020
Review #1 received
Received 23 Jun, 2020
Review #4 received
Received 23 Jun, 2020
Reviewer #3 agreed
On 19 Jun, 2020
Reviewer #2 agreed
On 18 Jun, 2020
Editor assigned
On 17 Jun, 2020
Reviewers invited
Invitations sent on 17 Jun, 2020
Reviewer #1 agreed
On 17 Jun, 2020
Submission checks complete
On 16 Jun, 2020
Editor invited
On 16 Jun, 2020
No comments provided
Editor assigned
On 08 Jun, 2020
Editorial decision: Revise Before Review
On 08 Jun, 2020
Submission checks complete
On 07 Jun, 2020
Editor invited
On 07 Jun, 2020
Version 1
Posted 13 Feb, 2020
No comments provided
Editorial decision: Major revision
On 03 Mar, 2020
Review #6 received
Received 02 Mar, 2020
Review #5 received
Received 28 Feb, 2020
Review #3 received
Received 26 Feb, 2020
Review #4 received
Received 26 Feb, 2020
Reviewer #6 agreed
On 17 Feb, 2020
Review #2 received
Received 17 Feb, 2020
Review #1 received
Received 17 Feb, 2020
Reviewer #3 agreed
On 14 Feb, 2020
Reviewer #4 agreed
On 14 Feb, 2020
Reviewer #5 agreed
On 14 Feb, 2020
Reviewers invited
Invitations sent on 14 Feb, 2020
Reviewer #1 agreed
On 14 Feb, 2020
Reviewer #2 agreed
On 14 Feb, 2020
Editor assigned
On 13 Feb, 2020
Editor invited
On 12 Feb, 2020
First submitted
On 11 Feb, 2020
Submission checks complete
On 11 Feb, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Critical Care & Emergency Medicine
License:
This work is licensed under a CC BY 4.0 License. Read Full License
View the published article at Cancer Cell International.
Background: Endometrial cancer is one of the most common cancers affecting women's health. The pathogenesis of endometrial cancer involves many signaling pathways which are related with transcription factors or microRNAs. Recent studies have reported that endometrial cancer is also related with the sexual-mediated hormones. The purpose of this research is to treat the endometrial cancer with the hormone-related drugs, and find out the specific molecular mechanism.
Methods: In this study, RL95-2 cells and Ishikawa cells were used as the endometrial cancer cell models. miR-492 was transfected into RL95-2 cells and Ishikawa cells. The miRNA expression was measured by qRT-PCR. The protein expression was measured by western blot. Cell proliferation was monitored using the MTT assay and cell colony formation assay. Cell apoptosis was monitored using EdU assay.
Results: Firstly, the results indicated that metapristone as a kind of hormone-related drugs could significantly inhibit the endometrial cancer cell growth through regulating cell apoptosis-related gene expression. Meanwhile, miR-492 was detected to be highly expressed in the endometrial cancer cell lines. Overexpression of miR-492 could promote the cell proliferation and inhibit the cell apoptosis. Furthermore, the results demonstrated that the downstream target genes of miR-492 were Klf5 and Nrf1, which were inhibited by metapristone. At the animal level, metapristone also inhibited the endometrial cancer cell growth through down-regulating the expression of miR-492 and decreasing the protein level of Klf5 and Nrf1.
Conclusion: Taken together, this study indicated that metapristone inhibited the endometrial cancer cell growth through regulating the cell apoptosis related signaling pathway and the expression of miR-492 and its downstream target genes (Klf5 and Nrf1), which provided the theoretical basis of endometrial cancer in clinical treatment.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
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