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  • Open Access

    ARTICLE

    NET1 Enhances Proliferation and Chemoresistance in Acute Lymphoblastic Leukemia Cells

    Hongbo Sun*1, Zhifu Zhang*1, Wei Luo*, Junmin Liu*, Ye Lou, Shengmei Xia

    Oncology Research, Vol.27, No.8, pp. 935-944, 2019, DOI:10.3727/096504019X15555388198071

    Abstract Acute lymphoblastic leukemia (ALL) is the most prevalent of pediatric cancers. Neuroepithelial cell-transforming 1 (NET1) has been associated with malignancy in a number of cancers, but the role of NET1 in ALL development is unclear. In the present study, we investigated the effect of NET1 gene in ALL cell proliferation and chemoresistance. We analyzed GEO microarray data comparing bone marrow expression profiles of pediatric B-cell ALL samples and those of age-matched controls. MTT and colony formation assays were performed to analyze cell proliferation. ELISA assays, Western blot analyses, and TUNEL staining were used to detect chemoresistance. We confirmed that NET1… More >

  • Open Access

    ARTICLE

    PPARb/d Agonist GW501516 Inhibits Tumorigenesis and Promotes Apoptosis of the Undifferentiated Nasopharyngeal Carcinoma C666-1 Cells by Regulating miR-206

    Linglan Gu, Yi Shi, Weimin Xu, Yangyang Ji

    Oncology Research, Vol.27, No.8, pp. 923-933, 2019, DOI:10.3727/096504019X15518706875814

    Abstract In previous investigations, we reported that peroxisome proliferator-activated receptor / (PPAR / ) activation by GW501516 inhibits proliferation and promotes apoptosis in the undifferentiated C666-1 nasopharyngeal carcinoma (NPC) cells by modulating caspase-dependent apoptotic pathway. In the present study, the mechanism by which GW501516 induces apoptosis was explored from the perspective of microRNA (miRNA) expression. Among the assayed miRNAs that were involved in regulating the expression of antiapoptotic protein Bcl-2, miR-206 was increased significantly and specifically by GW501516 in C666-1 cells at both the in vitro level and at the in vivo xenograft samples. The induction on miR-206 expression caused by… More >

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