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Primary research
Xu JianBo
Department of Hepatobiliary Surgery, The Affiliated Huaian NO.1 People’s Hospital of Nanjing Medical University, Huai’an, Jiangsu Province, P. R. China. 223001
Corresponding Author
ORCiD: https://orcid.org/0000-0002-1470-7264
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: PR55α plays important roles in oncogenesis and progression of numerous malignancies. However, its role in hepatocellular carcinoma (HCC) is unclear.
Methods: PR55α expressions in HCC tissues and paired healthy liver samples were detected using Western blot and tissue microarray immunohistochemistry. We knocked down the expression of PR55α in SMMC-7721 and LM3 cell lines via small interfering and lentivirus. In vitro cell counting, colony formation, migration and invasion assays were performed along with in vivo xenograft implantation and lung metastases experiments. The potential mechanisms involving target signal pathways were investigated by RNA-sequencing.
Results: PR55α expression level was suppressed in HCC tissues in comparison to healthy liver samples and was indicative of poorer prognosis. Knockdown of PR55α significantly promoted cell proliferation and migration, induced repression of the cell cycle progression and apoptosis in vitro while accelerating in vivo HCC growth and metastasis. Mechanistic analysis indicated that PR55α silencing was involved with MAPK/AKT signal pathway activation and resulted in increased phosphorylation of both AKT and ERK1/2.
Conclusion: This study identifies PR55α to be a candidate novel therapeutic target in the treatment of HCC.
Keywords
Hepatocellular Carcinoma, PR55α, Cell Proliferation, Cancer Metastasis
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CURRENT STATUS: Published
View the published article at Cancer Cell International.
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Editorial decision: Accept
On 24 Jan, 2021
Editor assigned
On 21 Jan, 2021
Review #2 received
Received 21 Jan, 2021
Submission checks complete
On 21 Jan, 2021
Editor invited
On 21 Jan, 2021
Reviewer #2 agreed
On 20 Jan, 2021
Reviewers invited
Invitations sent on 20 Jan, 2021
Reviewer #1 agreed
On 20 Jan, 2021
Review #1 received
Received 20 Jan, 2021
Version 1
Posted 07 Jan, 2021
No comments provided
Editorial decision: Major revision
On 03 Jan, 2021
Review #2 received
Received 02 Jan, 2021
Reviewer #2 agreed
On 01 Jan, 2021
Review #1 received
Received 01 Jan, 2021
Reviewers invited
Invitations sent on 31 Dec, 2020
Reviewer #1 agreed
On 31 Dec, 2020
Editor assigned
On 30 Dec, 2020
Submission checks complete
On 30 Dec, 2020
Editor invited
On 30 Dec, 2020
First submitted
On 28 Dec, 2020
Metrics
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PDF Downloads: ...
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Subject Areas
Cancer Biology
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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 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
Xu JianBo
Department of Hepatobiliary Surgery, The Affiliated Huaian NO.1 People’s Hospital of Nanjing Medical University, Huai’an, Jiangsu Province, P. R. China. 223001
Corresponding Author
ORCiD: https://orcid.org/0000-0002-1470-7264
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 Cancer Cell International.
No community comments so far
Editorial decision: Accept
On 24 Jan, 2021
Editor assigned
On 21 Jan, 2021
Review #2 received
Received 21 Jan, 2021
Submission checks complete
On 21 Jan, 2021
Editor invited
On 21 Jan, 2021
Reviewer #2 agreed
On 20 Jan, 2021
Reviewers invited
Invitations sent on 20 Jan, 2021
Reviewer #1 agreed
On 20 Jan, 2021
Review #1 received
Received 20 Jan, 2021
Version 1
Posted 07 Jan, 2021
No comments provided
Editorial decision: Major revision
On 03 Jan, 2021
Review #2 received
Received 02 Jan, 2021
Reviewer #2 agreed
On 01 Jan, 2021
Review #1 received
Received 01 Jan, 2021
Reviewers invited
Invitations sent on 31 Dec, 2020
Reviewer #1 agreed
On 31 Dec, 2020
Editor assigned
On 30 Dec, 2020
Submission checks complete
On 30 Dec, 2020
Editor invited
On 30 Dec, 2020
First submitted
On 28 Dec, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Cancer Biology
License:
This work is licensed under a CC BY 4.0 License. Read Full License
View the published article at Cancer Cell International.
Background: PR55α plays important roles in oncogenesis and progression of numerous malignancies. However, its role in hepatocellular carcinoma (HCC) is unclear.
Methods: PR55α expressions in HCC tissues and paired healthy liver samples were detected using Western blot and tissue microarray immunohistochemistry. We knocked down the expression of PR55α in SMMC-7721 and LM3 cell lines via small interfering and lentivirus. In vitro cell counting, colony formation, migration and invasion assays were performed along with in vivo xenograft implantation and lung metastases experiments. The potential mechanisms involving target signal pathways were investigated by RNA-sequencing.
Results: PR55α expression level was suppressed in HCC tissues in comparison to healthy liver samples and was indicative of poorer prognosis. Knockdown of PR55α significantly promoted cell proliferation and migration, induced repression of the cell cycle progression and apoptosis in vitro while accelerating in vivo HCC growth and metastasis. Mechanistic analysis indicated that PR55α silencing was involved with MAPK/AKT signal pathway activation and resulted in increased phosphorylation of both AKT and ERK1/2.
Conclusion: This study identifies PR55α to be a candidate novel therapeutic target in the treatment of HCC.
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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