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Research Article
Kui Chen
The First Affiliated Hospital of Zhengzhou University
Corresponding Author
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Backgrounds
NCK1-AS1 promotes cervical cancer, while its involvement in esophageal cancer is hardly known. We therefore explored the involvement of NCK1-AS1 in esophageal squamous cell carcinoma (ESCC) and analyzed the possible interaction between NCK1-AS1 and TGF-β signaling.
Methods
Our study selected 52 cases (30 males and 22 females, 46 to 70 years, 56.4 ± 6.6 years) to be used as the research subjects in this study. RT-qPCR and western blot were used for gene expression analysis. Transient transfections were used to analyze gene interaction. Transwell assays were performed to analyze cell invasion and invasion.
Results
Our data showed that NCK1-AS1 was overexpressed in ESCC patients. NCK1-AS1 in plasma was positively correlated with the NCK1-AS1 in tumor but not in non-tumor tissues. High plasma levels of NCK1-AS1 were accompanied by poor survival. TGF-β1 expression level was also increased in tumor tissues compared to tumor adjacent normal tissues. TGF-β1 was positively correlated with NCK1-AS1 in tumor tissues. TGF-β1 overexpression did not affect NCK1-AS1 expression, while NCK1-AS1 upregulated TGF-β1 in ESCC cells. TGF-β1 and NCK1-AS1 increased ESCC cell migration and invasion, TGF-β inhibitor reduced the effects of NCK1-AS1 overexpression.
Conclusion
Therefore, NCK1-AS1 may promote ESCC by upregulating TGF-β1.
Keywords
esophageal squamous cell carcinoma, lncRNANCK1-AS1, TGF-β1, survival, regulation
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A new preprint design is coming!
We have improved readability, clarity, accessibility, and opportunities for engagement.
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
Kui Chen
The First Affiliated Hospital of Zhengzhou University
Corresponding Author
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 19 Jan, 2021
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Backgrounds
NCK1-AS1 promotes cervical cancer, while its involvement in esophageal cancer is hardly known. We therefore explored the involvement of NCK1-AS1 in esophageal squamous cell carcinoma (ESCC) and analyzed the possible interaction between NCK1-AS1 and TGF-β signaling.
Methods
Our study selected 52 cases (30 males and 22 females, 46 to 70 years, 56.4 ± 6.6 years) to be used as the research subjects in this study. RT-qPCR and western blot were used for gene expression analysis. Transient transfections were used to analyze gene interaction. Transwell assays were performed to analyze cell invasion and invasion.
Results
Our data showed that NCK1-AS1 was overexpressed in ESCC patients. NCK1-AS1 in plasma was positively correlated with the NCK1-AS1 in tumor but not in non-tumor tissues. High plasma levels of NCK1-AS1 were accompanied by poor survival. TGF-β1 expression level was also increased in tumor tissues compared to tumor adjacent normal tissues. TGF-β1 was positively correlated with NCK1-AS1 in tumor tissues. TGF-β1 overexpression did not affect NCK1-AS1 expression, while NCK1-AS1 upregulated TGF-β1 in ESCC cells. TGF-β1 and NCK1-AS1 increased ESCC cell migration and invasion, TGF-β inhibitor reduced the effects of NCK1-AS1 overexpression.
Conclusion
Therefore, NCK1-AS1 may promote ESCC by upregulating TGF-β1.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
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