Migration/Invasion of Malignant Gliomas and Implications for Therapeutic Treatment

Liu, Ching Ann; Chang, Chia Yu; Hsueh, Kuo Wei; Su, Hong; Chiou, Tzyy Wen; Lin, Shinn Zong; Harn, Horng Jyh

doi:10.3390/ijms19041115

Cited by 81 publications

(56 citation statements)

References 187 publications

(193 reference statements)

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“…Migration and invasion contribute to patients' death in glioma, and blocking cancer cell metastasis has been indicated as a promising avenue for therapeutic treatment [3]. A previous study has reported that the anesthetic technique and anesthetics have important impacts on cancer migration and invasion to influence the outcome of patients suffering from surgery treatment [4].…”

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: Sevoflurane suppresses migration and invasion of glioma cells by regulating miR-146b-5p and MMP16

Zhang

Wang

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Background: Glioma is the most common brain tumor with poor prognosis all over the world. Anesthetics have been demonstrated to have important impacts on cell migration and invasion in different cancers. However, the underlying mechanism that allows anesthetics-mediated progression of glioma cells remains elusive. Methods: Sevoflurane (Sev), a class of common anesthetics, was used to expose to U87-MG and U251 cells. The expressions of microRNA-146b-5p (miR-146b-5p) and matrix metallopeptidase 16 (MMP16)were measured by quantitative real-time polymerase chain reaction or western blot. Transfection was performed in glioma cells with miR-146b-5p inhibitor, inhibitor negative control, MMP16 overexpression vector, empty vector, small interfering RNA against MMP16 or scramble. Cell migration and invasion were analyzed by the trans-well assay. The interaction between miR-146b-5p and MMP16 was explored by luciferase activity and RNA immunoprecipitation assays. Results: Sev treatment inhibited migration and invasion of glioma cells. The expression of miR-146b-5p was enhanced and MMP16 protein was decreased in glioma cells after exposure of Sev. Knockdown of miR-146b-5p or overexpression of MMP16 reversed Sev-induced inhibition of migration and invasion of glioma cells. Moreover, MMP16 was indicated as a target of miR-146b-5p and its silencing attenuated the regulatory role of miR-146b-5p abrogationin Sev-treated glioma cells. Conclusion: Sev impeded cell migration and invasion through regulating miR-146b-5p and MMP16 in glioma, indicating a novel theories foundation for the application of anesthetics like Sev in glioma.

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Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: Sevoflurane suppresses migration and invasion of glioma cells by regulating miR-146b-5p and MMP16

Zhang

Wang

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…To explore whether KCNQ1OT1 could regulate RRM2 via miR-338-3p in glioma, A172 and U251 cells were transfected with pcDNA3.1, pcDNA3.1/KCNQ1OT1, pcDNA3.1/ KCNQ1OT1 and miR-NC or miR-338-3p. The data of qRT-PCR revealed that RRM2 mRNA levels were significantly major risk factors for malignant gliomas [28]. By using trans-well migration and invasion assays, we confirmed the anti-migratory and anti-invasive roles of KCNQ1OT1 knockdown in glioma cells.…”

Section: Overexpression Of Kcnq1ot1 Up-regulates Rrm2 Expression By Dsupporting

confidence: 58%

Knockdown of lncRNA KCNQ1OT1 inhibits glioma progression by regulating miR-338-3p/RRM2

et al. 2020

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AbstractThe dysregulated lncRNA play essential roles in glioma development. This study aimed to investigate the role and mechanism of lncRNA potassium voltage-gated channel subfamily Q member 1 opposite strand/ antisense transcript 1 (KCNQ1OT1) in glioma progression. Tumor tissues and adjacent normal samples were collected from 30 glioma patients. The expression levels of lncRNA KCNQ1OT1, microRNA (miR)-338-3p and ribonucleotide reductase M2 (RRM2) were detected by quantitative real-time polymerase chain reaction or western blot analyses. Levels of cell viability, apoptosis, cell migration and invasion in glioma cell lines were determined using cell counting kit-8, flow cytometry with annexin V-FITC and trans-well assays, respectively. The role of KCNQ1OT1 in glioma development in vivo was investigated using a xenograft model. The target association between miR-338-3p and KCNQ1OT1 or RRM2 was validated by luciferase reporter assay. The results found that expression of KCNQ1OT1 was enhanced in glioma tissues and cells, and KCNQ1OT1 knockdown inhibited cell viability, migration and invasion, and xenograft tumor growth, but promoted apoptosis. miR-338-3p was targeted via KCNQ1OT1 and could reverse the effect of KCNQ1OT1 on glioma progression. RRM2 was targeted via miR-338-3p and attenuated the suppressive effect of miR-338-3p on glioma cell viability, migration and invasion. Besides, KCNQ1OT1 overexpression increased RRM2 expression, and this event was weakened via miR-338-3p up-regulation. In conclusion, the present finding suggest that silencing of KCNQ1OT1 can suppress the development and progression of glioma by up-regulating miR-338-3p and down-regulating RRM2.

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“…This poor prognosis is due, in part, to the diffusive invasive growth of GBM cells, which prevents the possibility of complete resection and limits the effect of local radiotherapy (Naumman et al 2013;Memmel et al 2017). Poor prognosis can also be attributed to large inter-and intratumoral heterogeneity, wherein tumor subpopulations associated with different molecular characteristics develop resistance to radiation and chemotherapies (Liu et al 2018;Akgül et al 2019). Various molecular characteristics have been associated with distinct GBM subtypes, and studies have increasingly shown that molecular profiling can be used to identify clinically relevant tumor subtypes and aid in treatment decisions (Verhaak et al 2010;Ceccarelli et al 2016; Barthel et al 2018).…”

Section: Introductionmentioning

confidence: 99%

Molecular and clonal evolution in recurrent metastatic gliosarcoma

Anderson

Tan

Parkinson

et al. 2020

Cold Spring Harb Mol Case Stud

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We discuss the molecular evolution of gliosarcoma, a mesenchymal type of glioblastoma (GBM), using the case of a 37-yr-old woman who developed two recurrences and an extracranial metastasis. She was initially diagnosed with isocitrate dehydrogenase (IDH) wild-type gliosarcoma in the frontal lobe and treated with surgery followed by concurrent radiotherapy with temozolomide. Five months later the tumor recurred in the left frontal lobe, outside the initially resected area, and was treated with further surgery and radiotherapy. Six months later the patient developed a second left frontal recurrence and was again treated with surgery and radiotherapy. Six weeks later, further recurrence was observed in the brain and bone, and biopsy confirmed metastases in the pelvic bones. To understand the clonal relationships between the four tumor instances and the origin of metastasis, we performed whole-genome sequencing of the intracranial tumors and the tumor located in the right iliac bone. We compared their mutational and copy-number profiles and inferred the clonal phylogeny. The tumors harbored shared alterations in GBM driver genes, including mutations in TP53, NF1, and RB1, and CDKN2A deletion. Whole-genome doubling was identified in the first recurrence and the extracranial metastasis. Comparisons of the metastatic to intracranial tumors highlighted a high similarity in molecular profile but contrasting evidence regarding the origin of the metastasis. Subclonal reconstruction suggested a parallel evolution of the recurrent tumors, and that the metastatic tumor was largely derived from the first recurrence. We conclude that metastasis in glioma can be a late event in tumorigenesis.

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Migration/Invasion of Malignant Gliomas and Implications for Therapeutic Treatment

Cited by 81 publications

References 187 publications

RETRACTED ARTICLE: Sevoflurane suppresses migration and invasion of glioma cells by regulating miR-146b-5p and MMP16

RETRACTED ARTICLE: Sevoflurane suppresses migration and invasion of glioma cells by regulating miR-146b-5p and MMP16

Knockdown of lncRNA KCNQ1OT1 inhibits glioma progression by regulating miR-338-3p/RRM2

Molecular and clonal evolution in recurrent metastatic gliosarcoma

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