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LncRNA ZFAS1 promotes pancreatic adenocarcinoma metastasis via the RHOA/ROCK2 pathway by sponging miR-3924
Chunlin Ge
The Fisrt Affiliated Hospital of China Medical University
Corresponding Author
ORCiD: https://orcid.org/0000-0001-7413-435X
License:
This work is licensed under a CC BY 4.0 License. Read Full License
View the published version at Cancer Cell International.
Background: The mortality and morbidity rates of pancreatic adenocarcinoma have been increasing over the past two decades, and an understanding of the mechanisms underlying pancreatic adenocarcinoma progression is urgently needed. The long non-coding RNA ZFAS1 has been demonstrated to be an oncogene in some cancers, but its function and mechanism in pancreatic adenocarcinoma remain unclear.
Methods: The ZFAS1 expression level in pancreatic adenocarcinoma was predicted by bioinformatic analysis, and the expression level of ZFAS1 in pancreatic adenocarcinoma tissue samples and cell lines was further investigated by quantitative real-time PCR and in situ hybridization. The functions of ZFAS1 in pancreatic adenocarcinoma in vitro and in vivo were investigated by further bioinformatic analysis. Dual-luciferase reporter assays were used to investigate the binding of ZFAS1/miR-3924 and miR-3924/ROCK2, and rescue assays were performed to further investigate the underlying mechanism.
Results: ZFAS1 overexpression in pancreatic adenocarcinoma was predicted and experimentally verified. ZFAS1 silencing inhibited pancreatic adenocarcinoma metastasis in vitro and in vivo. The competing endogenous RNA mechanism of ZFAS1 was also identified.
Conclusions: Our results demonstrated the promotive effect of ZFAS1 on pancreatic adenocarcinoma metastasis and suggested its potential role as a novel regulator of ROCK2.
Keywords
PAAD, long non-coding RNA, ZFAS1, miR-3924, ROCK2
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CURRENT STATUS: Published
Version 2
Posted 10 Jun, 2020
Published
On 16 Jun, 2020
No community comments so far
Editorial decision: Accept
On 02 Jun, 2020
Editor assigned
On 01 Jun, 2020
Reviewers invited
Invitations sent on 01 Jun, 2020
Reviewer #1 agreed
On 01 Jun, 2020
Reviewer #2 agreed
On 01 Jun, 2020
Review #2 received
Received 01 Jun, 2020
Review #1 received
Received 01 Jun, 2020
Submission checks complete
On 31 May, 2020
Editor invited
On 31 May, 2020
No comments provided
Editorial decision: Major revision
On 02 May, 2020
Review #2 received
Received 01 May, 2020
Review #1 received
Received 23 Apr, 2020
Reviewer #2 agreed
On 18 Apr, 2020
Reviewer #1 agreed
On 18 Apr, 2020
Editor assigned
On 15 Apr, 2020
Reviewers invited
Invitations sent on 15 Apr, 2020
Editor invited
On 14 Apr, 2020
Submission checks complete
On 08 Apr, 2020
First submitted
On 07 Apr, 2020
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This preprint is under consideration at Cancer Cell International. A preprint is 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
LncRNA ZFAS1 promotes pancreatic adenocarcinoma metastasis via the RHOA/ROCK2 pathway by sponging miR-3924
Chunlin Ge
The Fisrt Affiliated Hospital of China Medical University
Corresponding Author
ORCiD: https://orcid.org/0000-0001-7413-435X
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
Version 2
Posted 10 Jun, 2020
Published
On 16 Jun, 2020
No community comments so far
Editorial decision: Accept
On 02 Jun, 2020
Editor assigned
On 01 Jun, 2020
Reviewers invited
Invitations sent on 01 Jun, 2020
Reviewer #1 agreed
On 01 Jun, 2020
Reviewer #2 agreed
On 01 Jun, 2020
Review #2 received
Received 01 Jun, 2020
Review #1 received
Received 01 Jun, 2020
Submission checks complete
On 31 May, 2020
Editor invited
On 31 May, 2020
No comments provided
Editorial decision: Major revision
On 02 May, 2020
Review #2 received
Received 01 May, 2020
Review #1 received
Received 23 Apr, 2020
Reviewer #2 agreed
On 18 Apr, 2020
Reviewer #1 agreed
On 18 Apr, 2020
Editor assigned
On 15 Apr, 2020
Reviewers invited
Invitations sent on 15 Apr, 2020
Editor invited
On 14 Apr, 2020
Submission checks complete
On 08 Apr, 2020
First submitted
On 07 Apr, 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 version at Cancer Cell International.
Background: The mortality and morbidity rates of pancreatic adenocarcinoma have been increasing over the past two decades, and an understanding of the mechanisms underlying pancreatic adenocarcinoma progression is urgently needed. The long non-coding RNA ZFAS1 has been demonstrated to be an oncogene in some cancers, but its function and mechanism in pancreatic adenocarcinoma remain unclear.
Methods: The ZFAS1 expression level in pancreatic adenocarcinoma was predicted by bioinformatic analysis, and the expression level of ZFAS1 in pancreatic adenocarcinoma tissue samples and cell lines was further investigated by quantitative real-time PCR and in situ hybridization. The functions of ZFAS1 in pancreatic adenocarcinoma in vitro and in vivo were investigated by further bioinformatic analysis. Dual-luciferase reporter assays were used to investigate the binding of ZFAS1/miR-3924 and miR-3924/ROCK2, and rescue assays were performed to further investigate the underlying mechanism.
Results: ZFAS1 overexpression in pancreatic adenocarcinoma was predicted and experimentally verified. ZFAS1 silencing inhibited pancreatic adenocarcinoma metastasis in vitro and in vivo. The competing endogenous RNA mechanism of ZFAS1 was also identified.
Conclusions: Our results demonstrated the promotive effect of ZFAS1 on pancreatic adenocarcinoma metastasis and suggested its potential role as a novel regulator of ROCK2.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6