TAO WANG
Articles written in Journal of Biosciences
Volume 40 Issue 3 September 2015 pp 477-485 Articles
Porcine circovirus type 2 ORF4 protein binds heavy chain ferritin
Qizhuang Lv Kangkang Guo Tao Wang Chengcheng Zhang Yanming Zhang
Porcine circovirus type 2 (PCV2) is the primary infectious agent of PCV-associated disease (PCVAD) in swine. ORF4 protein is a newly identified viral protein of PCV2 and is involved in virus-induced apoptosis. However, the molecular mechanisms of ORF4 protein regulation of apoptosis remain unclear, especially given there is no information regarding any cellular partners of the ORF4 protein. Here, we have utilized the yeast two-hybrid assay and identified four host proteins (FHC, SNRPN, COX8A and Lamin C) interacting with the ORF4 protein. Specially, FHC was chosen for further characterization due to its important role in apoptosis. GST pull-down, subcellular co-location and co-immunoprecipitation assays confirmed that the PCV2 ORF4 protein indeed interacted with the heavy-chain ferritin, which is an interesting clue that will allow us to determine the role of the ORF4 protein in apoptosis.
Volume 46 All articles Published: 12 November 2021 Article ID 0098 Article
DUO TIAN LAIFU LUO TAO WANG JIAN QIAO
MicroRNAs (miRNAs) have been demonstrated to play critical roles in the tumorigenesis of triple-negative breast cancer (TNBC). In this work, we addressed the specific role of miR-296-3p in TNBC. The levels ofmiR-296-3p and SOX4 were determined using RT-qPCR. The function of miR-296-3p overexpression onTNBC cell proliferation, migration, invasion, cancer stem cell (CSC)-like properties, and Wnt pathwayactivation was investigated by MTT, EdU, wound healing, Transwell, sphere formation assays and westernblot. Mechanistic investigations, including luciferase reporter, RNA pull-down, and RIP assays, were conductedto explore the regulatory mechanisms of miR-296-3p. We found that miR-296-3p was downregulatedin TNBC tissues and cells. Overexpression of miR-296-3p suppressed TNBC cell proliferation, migration,invasion, and CSC-like properties. Furthermore, miR-296-3p could bind to SOX4 and negatively modulateSOX4 expression. In addition, miR-296-3p was verified to inhibit Wnt/beta-catenin pathway by downregulatingSOX4. Moreover, overexpression of SOX4 or activation of Wnt pathway rescued the miR-296-3p upregulation-mediated suppressive effect on cellular processes in TNBC. In conclusion, miR-296-3p inhibits Wnt/beta-catenin pathway by targeting SOX4 and exerts anti-tumor effects in TNBC.
Volume 48, 2023
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