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  • Open Access

    ARTICLE

    The FN1-ITGB4 Axis Drives Acquired Chemoresistance in Bladder Cancer by Activating FAK Signaling

    Xiaoyu Zhang1,#, RenFei Zong1,#, Yan Sun1, Nan Chen2, Kunyao Zhu1, Hang Tong1, Tinghao Li1, Junlong Zhu1, Zijia Qin1, Linfeng Wu1, Aimin Wang1, Weiyang He1,*

    Oncology Research, Vol.34, No.2, 2026, DOI:10.32604/or.2025.072084 - 19 January 2026

    Abstract Objective: While cisplatin-based chemotherapy is pivotal for advanced bladder cancer, acquired resistance remains a major obstacle. This study investigates key molecular drivers of this resistance and potential reversal strategies. Methods: We established GC (Gemcitabine and Cisplatin)-resistant T24-R and UC3-R cell lines from T24 and UM-UC-3 (UC3) cells. Transcriptomic and proteomic analyses identified differentially expressed molecules. Apoptosis and cell viability were assessed by flow cytometry and CCK-8 (Cell Counting Kit-8) assays, while RT-qPCR (Reverse Transcription Quantitative Polymerase Chain Reaction) and Western blot analyzed gene and protein expression. Immunofluorescence evaluated FAK (Focal Adhesion Kinase) phosphorylation, and a… More >

  • Open Access

    ARTICLE

    IKIP downregulates THBS1/FAK signaling to suppress migration and invasion by glioblastoma cells

    ZHAOYING ZHU1,#, YANJIA HU2,#, FENG YE2, HAIBO TENG2, GUOLIANG YOU1, YUNHUI ZENG2, MENG TIAN2, JIANGUO XU2, JIN LI2, ZHIYONG LIU2, HAO LIU2,*, NIANDONG ZHENG1,*

    Oncology Research, Vol.32, No.7, pp. 1173-1184, 2024, DOI:10.32604/or.2024.042456 - 20 June 2024

    Abstract Background: Inhibitor of NF-κB kinase-interacting protein (IKIP) is known to promote proliferation of glioblastoma (GBM) cells, but how it affects migration and invasion by those cells is unclear. Methods: We compared levels of IKIP between glioma tissues and normal brain tissue in clinical samples and public databases. We examined the effects of IKIP overexpression and knockdown on the migration and invasion of GBM using transwell and wound healing assays, and we compared the transcriptomes under these different conditions to identify the molecular mechanisms involved. Results: Based on data from our clinical samples and from public databases, More >

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