See the published version of this preprint at Molecular Medicine.
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Background: LncRNA can regulate gene at various levels such as apparent genetics, alternative splicing, and regulation of mRNA degradation. However, the molecular mechanism of LncRNA in cholangiocarcinoma is still unclear. This deserves further exploration.
Methods:We investigated the expression of AGAP2-AS1 in 32 CCA tissues and two CCA cell lines. We found a LncRNA AGAP2-AS1 which induced by SP1 has not been reported in CCA, and Knockdown and overexpression were used to investigate the biological role of AGAP2-AS1 in vitro. CHIP and RIP were performed to verify the putative targets of AGAP2-AS1.
Results:AGAP2-AS1 was significantly upregulated in CCA tumor tissues.SP1 induced AGAP2-AS1 plays an important role in tumorigenesis. AGAP2-AS1 knockdown significantly inhibited proliferation and caused apoptosis in CCA cells. In addition, we demonstrated that AGAP2-AS1 promotes the proliferation of CCA.
Conclusions: We conclude that the long non-coding RNA AGAP2-AS1 plays a role in promoting the proliferation of cholangiocarcinoma.
Keywords
LncRNA, AGAP2-AS1, CCA, EZH2, Biomarker, Apoptosis
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CURRENT STATUS: Published
View the published article at Molecular Medicine.
Version 2
Posted 17 Sep, 2020
No community comments so far
Editorial decision: Accept
On 28 Sep, 2020
Review #1 received
Received 25 Sep, 2020
Editor assigned
On 16 Sep, 2020
Reviewers invited
Invitations sent on 16 Sep, 2020
Reviewer #1 agreed
On 16 Sep, 2020
Submission checks complete
On 15 Sep, 2020
Editor invited
On 15 Sep, 2020
No comments provided
Review #2 received
Received 19 Jun, 2020
Editorial decision: Major revision
On 19 Jun, 2020
Reviewer #2 agreed
On 15 Jun, 2020
Review #1 received
Received 12 Jun, 2020
Reviewer #1 agreed
On 27 May, 2020
Editor assigned
On 20 May, 2020
Reviewers invited
Invitations sent on 20 May, 2020
Editor invited
On 19 May, 2020
Submission checks complete
On 14 May, 2020
First submitted
On 08 May, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Oncology
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See the published version of this preprint at Molecular Medicine.
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
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 Molecular Medicine.
Version 2
Posted 17 Sep, 2020
No community comments so far
Editorial decision: Accept
On 28 Sep, 2020
Review #1 received
Received 25 Sep, 2020
Editor assigned
On 16 Sep, 2020
Reviewers invited
Invitations sent on 16 Sep, 2020
Reviewer #1 agreed
On 16 Sep, 2020
Submission checks complete
On 15 Sep, 2020
Editor invited
On 15 Sep, 2020
No comments provided
Review #2 received
Received 19 Jun, 2020
Editorial decision: Major revision
On 19 Jun, 2020
Reviewer #2 agreed
On 15 Jun, 2020
Review #1 received
Received 12 Jun, 2020
Reviewer #1 agreed
On 27 May, 2020
Editor assigned
On 20 May, 2020
Reviewers invited
Invitations sent on 20 May, 2020
Editor invited
On 19 May, 2020
Submission checks complete
On 14 May, 2020
First submitted
On 08 May, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Oncology
License:
This work is licensed under a CC BY 4.0 License. Read Full License
View the published article at Molecular Medicine.
Background: LncRNA can regulate gene at various levels such as apparent genetics, alternative splicing, and regulation of mRNA degradation. However, the molecular mechanism of LncRNA in cholangiocarcinoma is still unclear. This deserves further exploration.
Methods:We investigated the expression of AGAP2-AS1 in 32 CCA tissues and two CCA cell lines. We found a LncRNA AGAP2-AS1 which induced by SP1 has not been reported in CCA, and Knockdown and overexpression were used to investigate the biological role of AGAP2-AS1 in vitro. CHIP and RIP were performed to verify the putative targets of AGAP2-AS1.
Results:AGAP2-AS1 was significantly upregulated in CCA tumor tissues.SP1 induced AGAP2-AS1 plays an important role in tumorigenesis. AGAP2-AS1 knockdown significantly inhibited proliferation and caused apoptosis in CCA cells. In addition, we demonstrated that AGAP2-AS1 promotes the proliferation of CCA.
Conclusions: We conclude that the long non-coding RNA AGAP2-AS1 plays a role in promoting the proliferation of cholangiocarcinoma.
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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