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  • Open Access

    ARTICLE

    UHMK1 Promotes Prostate Cancer Progression through a Positive Feedback Loop with MTHFD2

    Chi Zhang1,#, Xi Huang2,#, Cheng Hu1, Bowen Tang1, Jianjie Wu1, Zhuolun Sun1, Weian Zhu1, Xiangfu Zhou1, Hengjun Xiao1,*, Hua Wang1,*

    Oncology Research, Vol.33, No.9, pp. 2331-2351, 2025, DOI:10.32604/or.2025.065119 - 28 August 2025

    Abstract Background: U2AF homology motif kinase 1 (UHMK1) has been associated with RNA processing and protein phosphorylation, thereby influencing tumor progression. The study aimed to explore its regulatory mechanisms and biological functions in human prostate cancer (PCa). Methods: In this study, we systematically evaluated the expression and prognostic significance of UHMK1 in public databases, followed by validation through immunohistochemistry (IHC) in PCa specimens. Both gain-of-function and loss-of-function experiments were conducted to elucidate the role of UHMK1 in vitro and in vivo. Additionally, a series of molecular and biochemical assays were performed to investigate the regulatory mechanisms underlying UHMK1… More >

  • Open Access

    ARTICLE

    miR-92a Inhibits Proliferation and Induces Apoptosis by Regulating Methylenetetrahydrofolate Dehydrogenase 2 (MTHFD2) Expression in Acute Myeloid Leukemia

    Yueli Gu*, Jinchun Si, Xichun Xiao*, Ying Tian*, Shuo Yang*

    Oncology Research, Vol.25, No.7, pp. 1069-1079, 2017, DOI:10.3727/096504016X14829256525028

    Abstract Aberrant expression of microRNA-92a (miR-92a) has been investigated in various cancers. However, the function and mechanism of miR-92a in acute myeloid leukemia (AML) remain to be elucidated. Our data showed that miR-92a was evidently downregulated and methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) was remarkably upregulated in AML cell lines HL-60 and THP-1. Dual luciferase reporter assay revealed that MTHFD2 was a direct target of miR-92a. Gain- and loss-of-function analysis demonstrated that MTHFD2 knockdown or miR-92a overexpression notably inhibited proliferation and promoted apoptosis of AML cell lines. Restoration of MTHFD2 expression reversed proliferation inhibition and apoptosis induction of More >

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