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    Tumor-Suppressive MicroRNA-216b Binds to TPX2, Activating the p53 Signaling in Human Cutaneous Squamous Cell Carcinoma

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    Author
    Feng, C; Zhang, H-L; Zeng, A; Bai, M; Wang, X-J
    Date
    2020-06-05
    Source Title
    Molecular Therapy : Nucleic Acids
    Publisher
    CELL PRESS
    University of Melbourne Author/s
    Zhang, Lin
    Affiliation
    Medicine Dentistry & Health Sciences
    Metadata
    Show full item record
    Document Type
    Journal Article
    Citations
    Feng, C., Zhang, H. -L., Zeng, A., Bai, M. & Wang, X. -J. (2020). Tumor-Suppressive MicroRNA-216b Binds to TPX2, Activating the p53 Signaling in Human Cutaneous Squamous Cell Carcinoma. MOLECULAR THERAPY-NUCLEIC ACIDS, 20, pp.186-195. https://doi.org/10.1016/j.omtn.2020.01.022.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/251680
    DOI
    10.1016/j.omtn.2020.01.022
    Abstract
    Dysregulation of microRNAs (miRNAs) is acknowledged in human cutaneous squamous cell carcinoma (cSCC). We hereby evaluated the ability of miRNA-216b (miR-216b) to impact human cSCC. cSCC tissues with corresponding adjacent normal tissues were collected from 40 patients diagnosed with cSCC where the expression pattern of miR-216b and targeting protein for Xenopus kinesin-like protein 2 (TPX2) was determined by quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) and western blot analysis. A431 cells were transfected with miR-216b mimic, miR-216b inhibitor, or short interfering RNA against TPX2 to evaluate cell proliferation, invasion, migration, and apoptosis using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, scratch test, Transwell assay, and flow cytometry. TPX2 was highly expressed in cSCC tissues while miR-216b was poorly expressed in association with tumor differentiation, lymph node metastasis, and tumor node metastasis staging in patients with cSCC. In response to overexpressed miR-216b or silenced TPX2, cSCC cell proliferation, invasion, and migration were suppressed and apoptosis was stimulated, along with activated p53 signaling. Thus, upregulated miR-216b was capable of promoting apoptosis and inhibiting proliferation, invasion, and migration of cSCC cells by downregulating TPX2 through activation of the p53 signaling, highlighting a novel biomarker for novel treatment modalities against cSCC.

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