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Research article
Dong Ma
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Background: Epiplakin1 (Eppk1) is part of the EGF signal and is involved in cytoskeleton reorganization and cell proliferation. However, the role of Eppk1 in cervical cancer remains unknown.
Methods: The expression of Eppk1 and KLF5 as well as their correlation were assessed by RNA-seq, qRT-PCR, TCGA database and immunofluorescence staining. In CC cell lines, adenovirus-mediated overexpression or knockdown of KLF5 and Eppk1 as well as corresponding assessment of cell proliferation and signaling were determined by western blot and CCK8 experiments. Assays of lucifase reporter gene and CHIP were used to investigate mechanism between KLF5 and Eppk1.
Results: Eppk1 expression was markedly in CC tissues and cell lines companied by KLF5 upregulation. The results of immunofluorescence staining further showed that the increased expression of Eppk1 and KLF5 correlated with progression of cervical tumorigenesis. Overexpression of KLF5 significantly increased Eppk1 expression at transcription and translation levels. Conversely, the knockdown of KLF5 by siRNA against KLF5 decreased Eppk1 expression. Mechanical studies showed that KLF5 activated Eppk1 transcription by direct binding to the Eppk1 promoter. Gain- and loss-of-function experiments showed that KLF5 promoted cell proliferation in Hela by upregulating Eppk1 expression. Moreover, KLF5-mediated the activation of EGFR and p38 signaling significantly decreased after Eppk1 knockdown companied with reduction of proliferating activity, suggesting that Eppk1 lies upstream of p38 signaling affecting cell proliferation in CC. Finally, the expression of Eppk1 positively correlated with tumor size.
Conclusions: Eppk1 may be an effective therapeutic target on affecting EGFR-associated p38 signaling pathway and cell proliferation in cervical cancer.
Keywords
Cervical cancer, Eppk1, KLF5, proliferation, EGFR, p38 signal
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CURRENT STATUS: Published
View the published article at BMC Cancer.
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Reviewer #1 agreed
On 13 Dec, 2020
Reviewers invited
Invitations sent on 09 Dec, 2020
Editor assigned
On 06 Dec, 2020
Submission checks complete
On 06 Dec, 2020
Editor invited
On 06 Dec, 2020
Version 1
Posted 10 Jul, 2020
No comments provided
Editorial decision: Major revision
On 04 Nov, 2020
Review #2 received
Received 26 Oct, 2020
Reviewer #3 agreed
On 10 Oct, 2020
Reviewer #2 agreed
On 04 Oct, 2020
Review #1 received
Received 10 Sep, 2020
Reviewer #1 agreed
On 21 Aug, 2020
Reviewers invited
Invitations sent on 23 Jul, 2020
Editor assigned
On 21 Jul, 2020
Submission checks complete
On 09 Jul, 2020
Editor invited
On 09 Jul, 2020
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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
Dong Ma
Corresponding Author
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
Reviewer #1 agreed
On 13 Dec, 2020
Reviewers invited
Invitations sent on 09 Dec, 2020
Editor assigned
On 06 Dec, 2020
Submission checks complete
On 06 Dec, 2020
Editor invited
On 06 Dec, 2020
Version 1
Posted 10 Jul, 2020
No comments provided
Editorial decision: Major revision
On 04 Nov, 2020
Review #2 received
Received 26 Oct, 2020
Reviewer #3 agreed
On 10 Oct, 2020
Reviewer #2 agreed
On 04 Oct, 2020
Review #1 received
Received 10 Sep, 2020
Reviewer #1 agreed
On 21 Aug, 2020
Reviewers invited
Invitations sent on 23 Jul, 2020
Editor assigned
On 21 Jul, 2020
Submission checks complete
On 09 Jul, 2020
Editor invited
On 09 Jul, 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: Epiplakin1 (Eppk1) is part of the EGF signal and is involved in cytoskeleton reorganization and cell proliferation. However, the role of Eppk1 in cervical cancer remains unknown.
Methods: The expression of Eppk1 and KLF5 as well as their correlation were assessed by RNA-seq, qRT-PCR, TCGA database and immunofluorescence staining. In CC cell lines, adenovirus-mediated overexpression or knockdown of KLF5 and Eppk1 as well as corresponding assessment of cell proliferation and signaling were determined by western blot and CCK8 experiments. Assays of lucifase reporter gene and CHIP were used to investigate mechanism between KLF5 and Eppk1.
Results: Eppk1 expression was markedly in CC tissues and cell lines companied by KLF5 upregulation. The results of immunofluorescence staining further showed that the increased expression of Eppk1 and KLF5 correlated with progression of cervical tumorigenesis. Overexpression of KLF5 significantly increased Eppk1 expression at transcription and translation levels. Conversely, the knockdown of KLF5 by siRNA against KLF5 decreased Eppk1 expression. Mechanical studies showed that KLF5 activated Eppk1 transcription by direct binding to the Eppk1 promoter. Gain- and loss-of-function experiments showed that KLF5 promoted cell proliferation in Hela by upregulating Eppk1 expression. Moreover, KLF5-mediated the activation of EGFR and p38 signaling significantly decreased after Eppk1 knockdown companied with reduction of proliferating activity, suggesting that Eppk1 lies upstream of p38 signaling affecting cell proliferation in CC. Finally, the expression of Eppk1 positively correlated with tumor size.
Conclusions: Eppk1 may be an effective therapeutic target on affecting EGFR-associated p38 signaling pathway and cell proliferation in cervical cancer.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
This is a list of supplementary files associated with this preprint. Click to download.
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