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.
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Primary research
Ru-nan Zhang
Xinxiang Central Hospital
Corresponding Author
ORCiD: https://orcid.org/0000-0002-5458-406X
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: Emerging studies have attested that long noncoding RNAs (lncRNAs) predominantly functioned in carcinogenesis of multiple developing human tumors. The current research aimed at probing the underlying participation and mechanisms of LINC00337 in lung adenocarcinoma.
Methods: Here we analyzed TCGA and GTEx datasets and chose LINC00337 as research object. Cell proliferation, cell apoptosis, cell cycle, and invasion were detected in gain and loss experiment of LINC00337 both in vitro and in vivo. Moreover, RNA pull-down, luciferase reporter assays, western blotting analysis, rescue experiment were performed to investigate underlying molecular mechanisms of LINC00337 function.
Results: LINC00337 was remarkably increased in lung adenocarcinoma. Also, LINC00337 knock-down was unraveled to repress cell invasion and proliferation as well as cell cycle, and gear up apoptosis in lung adenocarcinoma in vitro and in vivo. With respect to mechanism, LINC00337 knock-down boosted miR-1285-3p to be expressed and then restrained YTHDF1 to be expressed post-transcriptionally. Crucially, both miR-1285-3p decrement and YTHDF1 overexpression successfully countered the influence on cell proliferation, invasion and apoptosis caused by LINC00337 shRNA.
Conclusions: These results suggest that LINC00337 acted as an oncogenic lncRNA, targeting miR-1285-3p and regulating YTHDF1 expression, to promote the progression of lung adenocarcinoma.
Keywords
lung adenocarcinoma, lncRNA, LINC00337, cell invasion, cell proliferation
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CURRENT STATUS: Under Revision
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On 18 Aug, 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
Ru-nan Zhang
Xinxiang Central Hospital
Corresponding Author
ORCiD: https://orcid.org/0000-0002-5458-406X
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: Under Revision
Version 1
Posted 11 Aug, 2020
No community comments so far
Editorial decision: Revise Before Review
On 18 Aug, 2020
Editor assigned
On 11 Aug, 2020
Editor invited
On 10 Aug, 2020
Submission checks complete
On 09 Aug, 2020
First submitted
On 08 Aug, 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
Background: Emerging studies have attested that long noncoding RNAs (lncRNAs) predominantly functioned in carcinogenesis of multiple developing human tumors. The current research aimed at probing the underlying participation and mechanisms of LINC00337 in lung adenocarcinoma.
Methods: Here we analyzed TCGA and GTEx datasets and chose LINC00337 as research object. Cell proliferation, cell apoptosis, cell cycle, and invasion were detected in gain and loss experiment of LINC00337 both in vitro and in vivo. Moreover, RNA pull-down, luciferase reporter assays, western blotting analysis, rescue experiment were performed to investigate underlying molecular mechanisms of LINC00337 function.
Results: LINC00337 was remarkably increased in lung adenocarcinoma. Also, LINC00337 knock-down was unraveled to repress cell invasion and proliferation as well as cell cycle, and gear up apoptosis in lung adenocarcinoma in vitro and in vivo. With respect to mechanism, LINC00337 knock-down boosted miR-1285-3p to be expressed and then restrained YTHDF1 to be expressed post-transcriptionally. Crucially, both miR-1285-3p decrement and YTHDF1 overexpression successfully countered the influence on cell proliferation, invasion and apoptosis caused by LINC00337 shRNA.
Conclusions: These results suggest that LINC00337 acted as an oncogenic lncRNA, targeting miR-1285-3p and regulating YTHDF1 expression, to promote the progression of lung adenocarcinoma.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
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