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      Study on the Inhibitory Effect of Curcumin on GBM and Its Potential Mechanism


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          Glioblastoma (GBM) is the most prevalent malignant tumor of the central nervous system (CNS). However, current GBM treatments are ineffective, signifying the great importance of exploring new therapeutic targets. Curcumin has been found to be a natural compound with an anticancer potential. However, its targets and mechanisms in GBM are still unclear.


          Differentially expressed genes (DEGs) were screened from the GBM dataset in the GEO database and intersected with the target genes of curcumin to select potential target genes. Subsequently, survival analysis was performed with the GEPIA database to confirm the effect of target genes on the prognosis of GBM, and functional enrichment analysis was performed using the DAVID database. In vitro, CCK-8 assay was used to screen the appropriate concentration of curcumin; scratch and transwell invasion assays were used to evaluate the effect of curcumin on the migration and invasion abilities of GBM cells. Furthermore, RT-qPCR and Western blotting were used to detect changes in target genes and flow cytometry was used to assess the apoptosis level.


          A total of 16 target genes of curcumin and GBM were obtained, among which ENO1, MMP2, and PRKD2 significantly affected the prognosis ( P < 0.05). We further selected ENO1 for functional enrichment analysis and found that it was enriched in the glycolytic pathway. Meanwhile, in vitro experiments showed that curcumin could inhibit the migration and invasion of U251 cells and promote apoptosis ( P < 0.05).


          ENO1 could be a possible target for curcumin in the suppression of GBM cells.

          Most cited references25

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          CBTRUS statistical report: Primary brain and central nervous system tumors diagnosed in the United States in 2006-2010.

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            Passenger Deletions Generate Therapeutic Vulnerabilities in Cancer

            Inactivation of tumor suppressor genes via homozygous deletion is a prototypic event in the cancer genome, yet such deletions often encompass neighboring genes. We hypothesized that homozygous deletions in such passenger genes can expose cancer-specific therapeutic vulnerabilities in the case where the collaterally deleted gene is a member of a functionally redundant family of genes exercising an essential function. The glycolytic gene Enolase 1 (ENO1) in the 1p36 locus is deleted in Glioblastoma (GBM), which is tolerated by expression of ENO2. We demonstrate that shRNA-mediated extinction of ENO2 selectively inhibits growth, survival, and tumorigenic potential of ENO1-deleted GBM cells and that the enolase inhibitor phosphonoacetohydroxamate (PhAH) is selectively toxic to ENO1-deleted GBM cells relative to ENO1-intact GBM cells or normal astrocytes. The principle of collateral vulnerability should be applicable to other passenger deleted genes encoding functionally-redundant essential activities and provide an effective treatment strategy for cancers harboring such genomic events.
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              Alpha-enolase as a potential cancer prognostic marker promotes cell growth, migration, and invasion in glioma

              Background The success of using glycolytic inhibitors for cancer treatment relies on better understanding the roles of each frequently deregulated glycolytic genes in cancer. This report analyzed the involvement of a key glycolytic enzyme, alpha-enolase (ENO1), in tumor progression and prognosis of human glioma. Methods ENO1 expression levels were examined in glioma tissues and normal brain (NB) tissues. The molecular mechanisms of ENO1 expression and its effects on cell growth, migration and invasion were also explored by 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT) assay, Transwell chamber assay, Boyden chamber assay, Western blot and in vivo tumorigenesis in nude mice. Results ENO1 mRNA and protein levels were upregulated in glioma tissues compared to NB. In addition, increased ENO1 was associated disease progression in glioma samples. Knocking down ENO1 expression not only significantly decreased cell proliferation, but also markedly inhibited cell migration and invasion as well as in vivo tumorigenesis. Mechanistic analyses revealed that Cyclin D1, Cyclin E1, pRb, and NF-κB were downregulated after stable ENO1 knockdown in glioma U251 and U87 cells. Conversely, knockdown of ENO1 resulted in restoration of E-cadherin expression and suppression of mesenchymal cell markers, such as Vimentin, Snail, N-Cadherin, β-Catenin and Slug. Furthermore, ENO1 suppression inactivated PI3K/Akt pathway regulating the cell growth and epithelial-mesenchymal transition (EMT) progression. Conclusion Overexpression of ENO1 is associated with glioma progression. Knockdown of ENO1 expression led to suppressed cell growth, migration and invasion progression by inactivating the PI3K/Akt pathway in glioma cells.

                Author and article information

                Drug Des Devel Ther
                Drug Des Devel Ther
                Drug Design, Development and Therapy
                28 June 2021
                : 15
                : 2769-2781
                [1 ]Department of Neurology, The First Affiliated Hospital of Guangxi Medical University , Nanning, 530021, People’s Republic of China
                [2 ]Department of Urology, The First Affiliated Hospital of Guangxi Medical University , Nanning, 530021, People’s Republic of China
                [3 ]Department of Ophthalmology, The First Affiliated Hospital of Guangxi Medical University , Nanning, 530021, People’s Republic of China
                Author notes
                Correspondence: Haoyu Li Department of Ophthalmology, The First Affiliated Hospital of Guangxi Medical University , 6 Shuangyong Road, Nanning, 530021, People’s Republic of China Email med.dr.lihy@gmail.com
                Chao Qin Department of Neurology, The First Affiliated Hospital of Guangxi Medical University , 6 Shuangyong Road, Nanning, 530021, People’s Republic of China Email mdqc2019@126.com
                Author information
                © 2021 Su et al.

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                : 14 February 2021
                : 03 June 2021
                Page count
                Figures: 11, Tables: 2, References: 25, Pages: 13
                Funded by: The National Natural Science Foundation of China;
                Funded by: the Science and Technology Plan Project of Guangxi;
                This work was supported by The National Natural Science Foundation of China (No. 81860222) and the Science and Technology Plan Project of Guangxi (No. AB16380204).
                Original Research

                Pharmacology & Pharmaceutical medicine
                glioblastoma,curcumin,eno1,migration,apoptosis,computational biology


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