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.
Research Article
Hao Zhang
Affiliated Hospital of Xuzhou Medical University
Corresponding Author
ORCiD: https://orcid.org/0000-0002-2926-737X
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background
As the most commonly diagnosed lung cancer, non–small cell lung carcinoma (NSCLC) is regulated by many long noncoding RNAs (lncRNAs). In the present study, we found that SH3PXD2A-AS1 expression in NSCLC tissues was upregulated compared with that in normal lung tissues in The Cancer Genome Atlas (TCGA) database. However, the role and molecular mechanism of SH3PXD2A-AS1 in NSCLC progression require further exploration.
Methods
The expression of SH3PXD2A-AS1 in NSCLC and normal lung tissues in a TCGA dataset was analysed by using the GEPIA website. K-M analysis was performed to explore the effects of this molecule on the survival rate in NSCLC. The functional characterization of the role and molecular mechanism of SH3PXD2A-AS1 in NSCLC was performed with a series of in vitro and in vivo experiments.
Results
SH3PXD2A-AS1 expression was increased in human NSCLC, and high SH3PXD2A-AS1 expression was correlated with poor overall survival. SH3PXD2A-AS1 overexpression sufficiently promoted tumour cell proliferation and accelerated cell cycle progression in vitro and tumour growth in vivo. Moreover, SH3PXD2A-AS1 interacted with DHX9 to enhance FOXM1 expression, promote tumour cell proliferation and accelerate cell cycle progression.
Conclusions
SH3PXD2A-AS1 promoted NSCLC growth by interacting with DHX9 to enhance FOXM1 expression. SH3PXD2A-AS1 may serve as a promising predictive biomarker for the diagnosis and prognosis of patients with NSCLC.
Keywords
SH3PXD2A-AS1, NSCLC, FOXM1, DHX9, Cell cycle
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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.
Research Article
Hao Zhang
Affiliated Hospital of Xuzhou Medical University
Corresponding Author
ORCiD: https://orcid.org/0000-0002-2926-737X
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 11 Mar, 2021
No community comments so far
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
As the most commonly diagnosed lung cancer, non–small cell lung carcinoma (NSCLC) is regulated by many long noncoding RNAs (lncRNAs). In the present study, we found that SH3PXD2A-AS1 expression in NSCLC tissues was upregulated compared with that in normal lung tissues in The Cancer Genome Atlas (TCGA) database. However, the role and molecular mechanism of SH3PXD2A-AS1 in NSCLC progression require further exploration.
Methods
The expression of SH3PXD2A-AS1 in NSCLC and normal lung tissues in a TCGA dataset was analysed by using the GEPIA website. K-M analysis was performed to explore the effects of this molecule on the survival rate in NSCLC. The functional characterization of the role and molecular mechanism of SH3PXD2A-AS1 in NSCLC was performed with a series of in vitro and in vivo experiments.
Results
SH3PXD2A-AS1 expression was increased in human NSCLC, and high SH3PXD2A-AS1 expression was correlated with poor overall survival. SH3PXD2A-AS1 overexpression sufficiently promoted tumour cell proliferation and accelerated cell cycle progression in vitro and tumour growth in vivo. Moreover, SH3PXD2A-AS1 interacted with DHX9 to enhance FOXM1 expression, promote tumour cell proliferation and accelerate cell cycle progression.
Conclusions
SH3PXD2A-AS1 promoted NSCLC growth by interacting with DHX9 to enhance FOXM1 expression. SH3PXD2A-AS1 may serve as a promising predictive biomarker for the diagnosis and prognosis of patients with NSCLC.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Figure 7
This is a list of supplementary files associated with this preprint. Click to download.
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