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Research article
Xiong Wang
Corresponding Author
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Background The pathogenesis of prolactinomas has not been clarified yet. p38 MAPK signaling including p38α MAPK (MAPK14), p38β (MAPK11), p38γ (MAPK12) and p38δ (MAPK13) is related to the development and progression of many cancers. We sought to investigate the role of MAPK14 in prolactinomas.
Methods Immunofluorescence assay was performed on the prolactin (PRL) and MAPK14 protein expressions of pituitary gland in C57BL/6 mice and human prolactinomas specimens. We analyzed the role of MAPK14 in prolactinomas using estradiol-induced model and DRD2-/- model in C57BL/6 wild-type (WT), MAPK14-/- , DRD2-/-MAPK14+/- mice. GH3 cells were transfected with different sets of MAPK14 siRNA, which to study MAPK14 and PRL protein expression in GH3.
Results Immunofluorescenc assaye found that PRL and MAPK14 were co-locatied and increased significantly in the pituitary gland of estradiol-injected prolactinomas mice than in control mice. And the deficiency of MAPK14 significantly inhibited the tumor overgrowth, along with the PRL decrease in estradiol-induced mice. Furthermore, MAPK14 deficiency in DRD2-/-MAPK14+/- mice significantly inhibited the overgrowth of pituitary gland and PRL production and secretion than in DRD2-/- mice. And MAPK14 knockdown by siRNA inhibited PRL production in GH3 cells.
Conclusion The results establish that MAPK14 plays a promoting role in the formation of prolactinomas, and validate MAPK14 as potential therapeutic target.
Keywords
Prolactinomas, Prolactin, MAPK14, DRD2
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CURRENT STATUS: Published
View the published article at BMC Endocrine Disorders.
No community comments so far
Submission checks complete
On 31 Aug, 2020
Editorial decision: Accept
On 28 Aug, 2020
No comments provided
Review #1 received
Received 10 Jul, 2020
Review #2 received
Received 30 Jun, 2020
Reviewer #2 agreed
On 27 Jun, 2020
Reviewer #1 agreed
On 24 Jun, 2020
Reviewers invited
Invitations sent on 24 Jun, 2020
Editor assigned
On 23 Jun, 2020
Submission checks complete
On 22 Jun, 2020
Editor invited
On 22 Jun, 2020
Version 1
Posted 01 May, 2020
No comments provided
Editorial decision: Major revision
On 01 Jun, 2020
Review #2 received
Received 30 May, 2020
Reviewer #2 agreed
On 03 May, 2020
Review #1 received
Received 01 May, 2020
Reviewers invited
Invitations sent on 30 Apr, 2020
Reviewer #1 agreed
On 30 Apr, 2020
Editor assigned
On 23 Apr, 2020
Submission checks complete
On 22 Apr, 2020
Editor invited
On 22 Apr, 2020
First submitted
On 21 Apr, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Endocrinology & Metabolism
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A new preprint design is coming!
We have improved readability, clarity, accessibility, and opportunities for engagement.
See the published version of this preprint at BMC Endocrine Disorders.
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
Xiong Wang
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 Endocrine Disorders.
No community comments so far
Submission checks complete
On 31 Aug, 2020
Editorial decision: Accept
On 28 Aug, 2020
No comments provided
Review #1 received
Received 10 Jul, 2020
Review #2 received
Received 30 Jun, 2020
Reviewer #2 agreed
On 27 Jun, 2020
Reviewer #1 agreed
On 24 Jun, 2020
Reviewers invited
Invitations sent on 24 Jun, 2020
Editor assigned
On 23 Jun, 2020
Submission checks complete
On 22 Jun, 2020
Editor invited
On 22 Jun, 2020
Version 1
Posted 01 May, 2020
No comments provided
Editorial decision: Major revision
On 01 Jun, 2020
Review #2 received
Received 30 May, 2020
Reviewer #2 agreed
On 03 May, 2020
Review #1 received
Received 01 May, 2020
Reviewers invited
Invitations sent on 30 Apr, 2020
Reviewer #1 agreed
On 30 Apr, 2020
Editor assigned
On 23 Apr, 2020
Submission checks complete
On 22 Apr, 2020
Editor invited
On 22 Apr, 2020
First submitted
On 21 Apr, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Endocrinology & Metabolism
License:
This work is licensed under a CC BY 4.0 License. Read Full License
View the published article at BMC Endocrine Disorders.
Background The pathogenesis of prolactinomas has not been clarified yet. p38 MAPK signaling including p38α MAPK (MAPK14), p38β (MAPK11), p38γ (MAPK12) and p38δ (MAPK13) is related to the development and progression of many cancers. We sought to investigate the role of MAPK14 in prolactinomas.
Methods Immunofluorescence assay was performed on the prolactin (PRL) and MAPK14 protein expressions of pituitary gland in C57BL/6 mice and human prolactinomas specimens. We analyzed the role of MAPK14 in prolactinomas using estradiol-induced model and DRD2-/- model in C57BL/6 wild-type (WT), MAPK14-/- , DRD2-/-MAPK14+/- mice. GH3 cells were transfected with different sets of MAPK14 siRNA, which to study MAPK14 and PRL protein expression in GH3.
Results Immunofluorescenc assaye found that PRL and MAPK14 were co-locatied and increased significantly in the pituitary gland of estradiol-injected prolactinomas mice than in control mice. And the deficiency of MAPK14 significantly inhibited the tumor overgrowth, along with the PRL decrease in estradiol-induced mice. Furthermore, MAPK14 deficiency in DRD2-/-MAPK14+/- mice significantly inhibited the overgrowth of pituitary gland and PRL production and secretion than in DRD2-/- mice. And MAPK14 knockdown by siRNA inhibited PRL production in GH3 cells.
Conclusion The results establish that MAPK14 plays a promoting role in the formation of prolactinomas, and validate MAPK14 as potential therapeutic target.
Figure 1
Figure 2
Figure 3
Figure 4
This is a list of supplementary files associated with this preprint. Click to download.
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