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Article

TMEM100 negatively regulated by microRNA‑106b facilitates cellular apoptosis by suppressing survivin expression in NSCLC

  • Authors:
    • Jun Ma
    • Tingting Yan
    • Yongrui Bai
    • Ming Ye
    • Chunhui Ma
    • Xiumei Ma
    • Lei Zhang
  • View Affiliations / Copyright

    Affiliations: Eye Institute, Eye and ENT Hospital, Shanghai Medical College, Fudan University, Shanghai 200031, P.R. China, Department of Breast Surgery, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, P.R. China, Department of Radiation Oncology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, P.R. China, Department of Orthopedic Surgery, Shanghai General Hospital, Shanghai Jiao Tong University, Shanghai 200080, P.R. China
  • Article Number: 185
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    Published online on: July 7, 2021
       https://doi.org/10.3892/or.2021.8136
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Abstract

Non‑small cell lung cancer (NSCLC) is a common malignant tumour. Nevertheless, the 5‑year survival rate of NSCLC patients remains poor. Thus, identifying critical factors involved in regulating the progression of NSCLC is important for providing potential treatment targets. In the present study, it was observed that transmembrane protein 100 (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 by suppressing survivin expression in NSCLC cells, whereas TMEM100 knockdown had the opposite effect. In addition, microRNA (miR)‑106b, a miR 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. The aforementioned results indicated that TMEM100 induced cell apoptosis and inhibited cell survival by serving as a tumour suppressor and that miR‑106b‑mitigatedTMEM100 expression defined a potentially oncogenic pathway in NSCLC.
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Copy and paste a formatted citation
Spandidos Publications style
Ma J, Yan T, Bai Y, Ye M, Ma C, Ma X and Zhang L: TMEM100 negatively regulated by microRNA‑106b facilitates cellular apoptosis by suppressing survivin expression in NSCLC. Oncol Rep 46: 185, 2021.
APA
Ma, J., Yan, T., Bai, Y., Ye, M., Ma, C., Ma, X., & Zhang, L. (2021). TMEM100 negatively regulated by microRNA‑106b facilitates cellular apoptosis by suppressing survivin expression in NSCLC. Oncology Reports, 46, 185. https://doi.org/10.3892/or.2021.8136
MLA
Ma, J., Yan, T., Bai, Y., Ye, M., Ma, C., Ma, X., Zhang, L."TMEM100 negatively regulated by microRNA‑106b facilitates cellular apoptosis by suppressing survivin expression in NSCLC". Oncology Reports 46.2 (2021): 185.
Chicago
Ma, J., Yan, T., Bai, Y., Ye, M., Ma, C., Ma, X., Zhang, L."TMEM100 negatively regulated by microRNA‑106b facilitates cellular apoptosis by suppressing survivin expression in NSCLC". Oncology Reports 46, no. 2 (2021): 185. https://doi.org/10.3892/or.2021.8136
Copy and paste a formatted citation
x
Spandidos Publications style
Ma J, Yan T, Bai Y, Ye M, Ma C, Ma X and Zhang L: TMEM100 negatively regulated by microRNA‑106b facilitates cellular apoptosis by suppressing survivin expression in NSCLC. Oncol Rep 46: 185, 2021.
APA
Ma, J., Yan, T., Bai, Y., Ye, M., Ma, C., Ma, X., & Zhang, L. (2021). TMEM100 negatively regulated by microRNA‑106b facilitates cellular apoptosis by suppressing survivin expression in NSCLC. Oncology Reports, 46, 185. https://doi.org/10.3892/or.2021.8136
MLA
Ma, J., Yan, T., Bai, Y., Ye, M., Ma, C., Ma, X., Zhang, L."TMEM100 negatively regulated by microRNA‑106b facilitates cellular apoptosis by suppressing survivin expression in NSCLC". Oncology Reports 46.2 (2021): 185.
Chicago
Ma, J., Yan, T., Bai, Y., Ye, M., Ma, C., Ma, X., Zhang, L."TMEM100 negatively regulated by microRNA‑106b facilitates cellular apoptosis by suppressing survivin expression in NSCLC". Oncology Reports 46, no. 2 (2021): 185. https://doi.org/10.3892/or.2021.8136
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