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  • FAM134B promotes esophageal squamous cell carcinoma in vitro and its correlations with clinicopathologic features

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    Islam178190.pdf (620.4Kb)
    Author(s)
    Islam, Farhadul
    Gopalan, Vinod
    Law, Simon
    Tang, Johnny Cheuk-on
    Lam, Alfred King-yin
    Griffith University Author(s)
    Gopalan, Vinod
    Lam, Alfred K.
    Islam, Farhad
    Year published
    2019
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    Abstract
    Family with sequence similarity 134, member B (FAM134B) is an autophagy regulator of endoplasmic reticulum first discovered to be involved in the pathogenesis of esophageal squamous cell carcinoma (ESCC). The present study examined the functional behavior of FAM134B in cancer cells and the association of FAM134B expression with clinicopathologic factors in patients with ESCC. Expression at both the mRNA and protein levels was investigated using real-time polymerase chain reaction and immunohistochemistry. The results were correlated with the clinical and pathological features of the patients. In addition, in vitro functional ...
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    Family with sequence similarity 134, member B (FAM134B) is an autophagy regulator of endoplasmic reticulum first discovered to be involved in the pathogenesis of esophageal squamous cell carcinoma (ESCC). The present study examined the functional behavior of FAM134B in cancer cells and the association of FAM134B expression with clinicopathologic factors in patients with ESCC. Expression at both the mRNA and protein levels was investigated using real-time polymerase chain reaction and immunohistochemistry. The results were correlated with the clinical and pathological features of the patients. In addition, in vitro functional assays were used to investigate the roles of FAM134B in ESCC cells in response to gene silencing with shRNA lentiviral particles. Overexpression of FAM134B mRNA and protein was present in 31.2% (n = 29/93) and 36.6% (n = 41/112), respectively, in tumors, whereas downregulation occurred in 39.8% (n = 37/93) and 63.4% (n = 71/112), respectively. Expression of FAM134B protein in ESCC correlated with histologic grade (P =.002) and pathologic stage (P =.012). In vitro suppression of FAM134B in ESCC induced significant reductions of cell proliferation and colony formation (P <.05). In addition, suppression of FAM134B caused reduction of wound healing, migration, and invasion capacities of ESCC. To conclude, FAM134B could play crucial roles in the initiation and progression of ESCC, and FAM134B protein expression has potential predictive value. Therefore, development of strategies targeting FAM134B could have therapeutic value in the management of patients with ESCC.
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    Journal Title
    HUMAN PATHOLOGY
    Volume
    87
    DOI
    https://doi.org/10.1016/j.humpath.2018.11.033
    Copyright Statement
    © 2019 Elsevier. Licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International Licence, which permits unrestricted, non-commercial use, distribution and reproduction in any medium, providing that the work is properly cited.
    Subject
    Clinical sciences
    Publication URI
    http://hdl.handle.net/10072/383663
    Collection
    • Journal articles

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