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Primary research
Lei Zhang
Shanghai Jiao Tong University School of Medicine Affiliated Renji Hospital
Corresponding Author
ORCiD: https://orcid.org/0000-0001-8102-3543
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background
Non-small-cell lung cancer (NSCLC) is a common malignant tumor. Nevertheless, the 5-year survival rate of NSCLC patients remains poor. Thus, finding critical factors involved in regulating the progression of NSCLC is important for providing potential treatment targets.
Methods
CCK-8, colony formation, caspase-3 activity, luciferase reporter assay, and western blot assays were utilized in this study.
Results
We found that TMEM100 was significantly downregulated in NSCLC tissues compared with paired peritumoral tissues. Decreased TMEM100 expression was associated with poor clinical outcomes in NSCLC patients. Moreover, TMEM100 overexpression inhibited colony formation and facilitated apoptosis via repressing survivin expression in NSCLC cells, whereas TMEM100 knockdown had the opposite effect. In addition, miR-106b, a microRNA with controversial roles in different human cancers, was upregulated in NSCLC and directly downregulated TMEM100 expression. The roles of miR-106b in cell survival were mitigated by the restoration of TMEM100.
Conclusions
The above results indicate that TMEM100 induces cell apoptosis and inhibits cell survival by serving as a tumor suppressor and that miR-106b-degraded TMEM100 expression defines a potentially oncogenic pathway in NSCLC.
Keywords
NSCLC, TMEM100, apoptosis, survival, miR-106b
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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.
Primary research
Lei Zhang
Shanghai Jiao Tong University School of Medicine Affiliated Renji Hospital
Corresponding Author
ORCiD: https://orcid.org/0000-0001-8102-3543
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 20 Feb, 2020
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
Background
Non-small-cell lung cancer (NSCLC) is a common malignant tumor. Nevertheless, the 5-year survival rate of NSCLC patients remains poor. Thus, finding critical factors involved in regulating the progression of NSCLC is important for providing potential treatment targets.
Methods
CCK-8, colony formation, caspase-3 activity, luciferase reporter assay, and western blot assays were utilized in this study.
Results
We found that TMEM100 was significantly downregulated in NSCLC tissues compared with paired peritumoral tissues. Decreased TMEM100 expression was associated with poor clinical outcomes in NSCLC patients. Moreover, TMEM100 overexpression inhibited colony formation and facilitated apoptosis via repressing survivin expression in NSCLC cells, whereas TMEM100 knockdown had the opposite effect. In addition, miR-106b, a microRNA with controversial roles in different human cancers, was upregulated in NSCLC and directly downregulated TMEM100 expression. The roles of miR-106b in cell survival were mitigated by the restoration of TMEM100.
Conclusions
The above results indicate that TMEM100 induces cell apoptosis and inhibits cell survival by serving as a tumor suppressor and that miR-106b-degraded TMEM100 expression defines a potentially oncogenic pathway in NSCLC.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
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