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  • 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

    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 >

  • Open Access

    REVIEW

    Molecularly Targeted Drugs Plus Radiotherapy and Temozolomide Treatment for Newly Diagnosed Glioblastoma: A Meta-Analysis and Systematic Review

    Jiahao Su*, Meiqin Cai*, Wensheng Li*, Bo Hou, Haiyong He, Cong Ling,Tengchao Huang, Huijiao Liu, Ying Guo*

    Oncology Research, Vol.24, No.2, pp. 117-128, 2016, DOI:10.3727/096504016X14612603423511

    Abstract Glioblastoma (GBM) is the most common primary malignant brain tumor that nearly always results in a bad prognosis. Temozolomide plus radiotherapy (TEM+RAD) is the most common treatment for newly diagnosed GBM. With the development of molecularly targeted drugs, several clinical trials were reported; however, the efficacy of the treatment remains controversial. So we attempted to measure the dose of the molecularly targeted drug that could improve the prognosis of those patients. The appropriate electronic databases (PubMed, MEDLINE, EMBASE, and the Cochrane Library) were searched for relevant studies. A meta-analysis was performed after determining which studies… More >

  • Open Access

    ARTICLE

    lncRNA MNX1-AS1 Promotes Glioblastoma Progression Through Inhibition of miR-4443

    Yan Gao, Yongchuan Xu, Jue Wang, Xue Yang, Lulu Wen, Juan Feng

    Oncology Research, Vol.27, No.3, pp. 341-347, 2019, DOI:10.3727/096504018X15228909735079

    Abstract Long noncoding RNAs (lncRNAs) have been acknowledged as important regulators in various human cancers. lncRNA MNX1-AS1 has been shown to be an oncogene in epithelial ovarian cancer. However, the function of MNX1-AS1 in glioblastoma (GBM) remains largely unknown. Here we found that the expression of MNX1-AS1 was significantly upregulated in GBM tissues and cell lines. Knockdown of MNX1-AS1 significantly inhibited the proliferation, migration, and invasion of GBM cells. In terms of mechanism, we found that MNX1-AS1 could bind to miR-4443 in GBM cells. Overexpression of miR-4443 significantly inhibited the expression of MNX1-AS1 and vice versa. More >

  • Open Access

    ARTICLE

    Long Noncoding RNA WEE2-AS1 Plays an Oncogenic Role in Glioblastoma by Functioning as a Molecular Sponge for MicroRNA-520f-3p

    Hengzhou Lin, Dahui Zuo, Jiabin He, Tao Ji, Jianzhong Wang, Taipeng Jiang

    Oncology Research, Vol.28, No.6, pp. 591-603, 2020, DOI:10.3727/096504020X15982623243955

    Abstract The long noncoding RNA WEE2 antisense RNA 1 (WEE2-AS1) plays an oncogenic role in hepatocellular carcinoma and triple negative breast cancer progression. In this study, we investigated the expression and roles of WEE2-AS1 in glioblastoma (GBM). Furthermore, the molecular mechanisms behind the oncogenic actions of WEE2-AS1 in GBM cells were explored in detail. WEE2-AS1 expression was detected using quantitative real-time polymerase chain reaction. The roles of WEE2-AS1 in GBM cells were evaluated by the cell counting kit-8 assay, flow cytometric analysis, Transwell cell migration and invasion assays, and tumor xenograft experiments. WEE2-AS1 expression was evidently… More >

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