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Search Results (26)
  • 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

    Knockdown of Ras-Related Protein 25 (Rab25) Inhibits the In Vitro Cytotoxicity and In Vivo Antitumor Activity of Human Glioblastoma Multiforme Cells

    Bingqian Ding1, Bei Cui1, Ming Gao, Zhenjiang Li, Chenyang Xu, Shaokang Fan, Weiya He

    Oncology Research, Vol.25, No.3, pp. 331-340, 2017, DOI:10.3727/096504016X14736286083065

    Abstract Ras-related protein 25 (Rab25) is a member of the Rab family, and it has been reported to play an important role in tumorigenesis. However, its direct involvement in human glioblastoma multiforme (GBM) is still unclear. The aim of the current study was to investigate the potential role of Rab25 in the growth, proliferation, invasion, and migration of human GBM. Our results showed that Rab25 expression was significantly higher in human GBM cell lines compared with a normal astrocyte cell line. In vitro functional studies revealed that knockdown of Rab25 reduced cell proliferation and inhibited invasion More >

  • Open Access

    ARTICLE

    Knockdown of Collagen Triple Helix Repeat Containing 1 (CTHRC1) Inhibits Epithelial–Mesenchymal Transition and Cellular Migration in Glioblastoma Cells

    Jianpeng Liu*, Wei Li, Shunshun Liu*, Xu Zheng*, Lin Shi*, Weitao Zhang*, Hongfa Yang*

    Oncology Research, Vol.25, No.2, pp. 225-232, 2017, DOI:10.3727/096504016X14732772150587

    Abstract Collagen triple helix repeat containing 1 (CTHRC1), an extracellular matrix-related protein, has been found to be upregulated in many solid tumors and contributes to tumorigenesis. We found that CTHRC1 is overexpressed in glioblastoma tissues and cells. By using the technique of RNA interference, the expression of CTHRC1 in the human glioblastoma U-87MG cell line was downregulated, and the proliferation and migration of U-87MG cells were examined. The results showed that the knockdown of CTHRC1 exerts inhibitory effects on the proliferation and migration ability of U-87MG cells. Knockdown of CTHRC1 expression in U-87MG cells resulted in More >

  • Open Access

    ARTICLE

    MicroRNA-598 Inhibits Cell Proliferation and Invasion of Glioblastoma by Directly Targeting Metastasis Associated in Colon Cancer-1 (MACC1)

    Ning Wang*1, Yang Zhang†1, Huaxin Liang

    Oncology Research, Vol.26, No.8, pp. 1275-1283, 2018, DOI:10.3727/096504018X15185735627746

    Abstract The dysregulation of microRNA (miRNA) expression is closely related with tumorigenesis and tumor development in glioblastoma (GBM). In this study, we found that miRNA-598 (miR-598) expression was significantly downregulated in GBM tissues and cell lines. Restoring miR-598 expression inhibited cell proliferation and invasion in GBM. Moreover, we validated that metastasis associated in colon cancer-1 (MACC1) is a novel target of miR-598 in GBM. Restoring MACC1 expression reversed the inhibitory effects of miR-598 overexpression on GBM cells. In addition, miR-598 overexpression suppressed Met/ AKT pathway activation in GBM. Our results provided compelling evidence that miR-598 serves More >

  • Open Access

    ARTICLE

    Oncogenic Role of MicroRNA-30b-5p in Glioblastoma Through Targeting Proline-Rich Transmembrane Protein 2

    Zhongjun Li*, Junxiu Guo*, Yujie Ma, Longbo Zhang, Zhixiong Lin*

    Oncology Research, Vol.26, No.2, pp. 219-230, 2018, DOI:10.3727/096504017X14944585873659

    Abstract MicroRNAs (miRs) have been found to play promoting or suppressive roles in different human cancers. However, the exact regulatory mechanism of miR-30b in glioblastoma remains unknown. Here we have shown that the expression of miR-30b is significantly increased in glioblastoma tissues and cell lines. Moreover, a high expression of miR-30b is significantly associated with a shorter survival time for glioblastoma patients. Knockdown of miR-30b caused a significant reduction in the proliferation, migration, and invasion of U87 and A172 cells. Proline-rich transmembrane protein 2 (PRRT2) was further identified as a novel target gene of miR-30b, and More >

  • Open Access

    ARTICLE

    CD103+ Cell Growth Factor Flt3L Enhances the Efficacy of Immune Checkpoint Blockades in Murine Glioblastoma Model

    Xiaolin Miao*1, Yiqi Chen*1, Ke Hao†1, Meiqin Zheng, Bingyu Chen, Kaiqiang Li, Ying Wang, Wei Zhang§, Yu Zhang§, Xiaozhou Mou§, Shanshan Jiang, Zhen Wang‡§

    Oncology Research, Vol.26, No.2, pp. 173-182, 2018, DOI:10.3727/096504017X14841698396865

    Abstract Glioblastoma is a lethal disease featuring a high proliferation of tumor cells, excessive angiogenesis, and heavy drug resistance. The overall survival of glioblastoma patients has been dismal, even with an intensive standard of care. Recent advances in immune checkpoint blockades are changing the treatment of cancers. However, the efficacy of immune checkpoint blockades in glioblastoma is still unclear. Here we investigated the roles of CD103+ cells in regulating the effect of immune checkpoint blockades in glioblastoma mouse models. Our findings indicated that the murine glioblastoma model was not sensitive to immune checkpoint blockades. Flt3L, a growth More >

  • Open Access

    ARTICLE

    The interplay mechanism between IDH mutation, MGMT-promoter methylation, and PRMT5 activity in the progression of grade 4 astrocytoma: unraveling the complex triad theory

    MAHER KURDI1,*, ALAA ALKHOTANI2, ABDULRAHMAN SABBAGH3, EYAD FAIZO4, AHMED I. LARY5, AHMED K. BAMAGA6, MAJID ALMANSOURI7, BADR HAFIZ8, THAMER ALSHARIF9, SALEH BAEESA8

    Oncology Research, Vol.32, No.6, pp. 1037-1045, 2024, DOI:10.32604/or.2024.051112

    Abstract Background: The dysregulation of Isocitrate dehydrogenase (IDH) and the subsequent production of 2-Hydroxyglutrate (2HG) may alter the expression of epigenetic proteins in Grade 4 astrocytoma. The interplay mechanism between IDH, O-6-methylguanine-DNA methyltransferase (MGMT)-promoter methylation, and protein methyltransferase proteins-5 (PRMT5) activity, with tumor progression has never been described. Methods: A retrospective cohort of 34 patients with G4 astrocytoma is classified into IDH-mutant and IDH-wildtype tumors. Both groups were tested for MGMT-promoter methylation and PRMT5 through methylation-specific and gene expression PCR analysis. Inter-cohort statistical significance was evaluated. Results: Both IDH-mutant WHO grade 4 astrocytomas (n = 22, 64.7%) and IDH-wildtype… More > Graphic Abstract

    The interplay mechanism between IDH mutation, MGMT-promoter methylation, and PRMT5 activity in the progression of grade 4 astrocytoma: unraveling the complex triad theory

  • Open Access

    REVIEW

    Targeting brain tumors with innovative nanocarriers: bridging the gap through the blood-brain barrier

    KARAN WADHWA1, PAYAL CHAUHAN1, SHOBHIT KUMAR2, RAKESH PAHWA3,*, RAVINDER VERMA4, RAJAT GOYAL5, GOVIND SINGH1, ARCHANA SHARMA6, NEHA RAO3, DEEPAK KAUSHIK1,*

    Oncology Research, Vol.32, No.5, pp. 877-897, 2024, DOI:10.32604/or.2024.047278

    Abstract Background: Glioblastoma multiforme (GBM) is recognized as the most lethal and most highly invasive tumor. The high likelihood of treatment failure arises from the presence of the blood-brain barrier (BBB) and stem cells around GBM, which avert the entry of chemotherapeutic drugs into the tumor mass. Objective: Recently, several researchers have designed novel nanocarrier systems like liposomes, dendrimers, metallic nanoparticles, nanodiamonds, and nanorobot approaches, allowing drugs to infiltrate the BBB more efficiently, opening up innovative avenues to prevail over therapy problems and radiation therapy. Methods: Relevant literature for this manuscript has been collected from a comprehensive More > Graphic Abstract

    Targeting brain tumors with innovative nanocarriers: bridging the gap through the blood-brain barrier

  • Open Access

    REVIEW

    A review on potential heterocycles for the treatment of glioblastoma targeting receptor tyrosine kinases

    NILAM BHUSARE, MAUSHMI KUMAR*

    Oncology Research, Vol.32, No.5, pp. 849-875, 2024, DOI:10.32604/or.2024.047042

    Abstract Glioblastoma, the most aggressive form of brain tumor, poses significant challenges in terms of treatment success and patient survival. Current treatment modalities for glioblastoma include radiation therapy, surgical intervention, and chemotherapy. Unfortunately, the median survival rate remains dishearteningly low at 12–15 months. One of the major obstacles in treating glioblastoma is the recurrence of tumors, making chemotherapy the primary approach for secondary glioma patients. However, the efficacy of drugs is hampered by the presence of the blood-brain barrier and multidrug resistance mechanisms. Consequently, considerable research efforts have been directed toward understanding the underlying signaling pathways… More > Graphic Abstract

    A review on potential heterocycles for the treatment of glioblastoma targeting receptor tyrosine kinases

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