scholarly journals Development of barcode and proteome profiling of glioblastoma

2014 ◽  
Vol 60 (3) ◽  
pp. 308-321 ◽  
Author(s):  
S.N. Naryzhny ◽  
N.L. Ronzhina ◽  
M.A. Mainskova ◽  
N.V. Belyakova ◽  
R.A. Pantina ◽  
...  
Keyword(s):  
Mass Spectrometry ◽  
Brain Tumor ◽  
Cell Lines ◽  
High Grade Glioma ◽  
Initial Step ◽  
High Grade ◽  
Glioblastoma Cell ◽  
Cancer Death ◽  
Annexin 1 ◽  
Glioblastoma Cell Lines

High grade glioma (glioblastoma) is the most common brain tumor. Its malignancy makes it the fourth biggest cause of cancer death. In our experiments we used several glioblastoma cell lines generated in our laboratory to obtain proteomics information specific for this disease. This study starts our developing the complete 2DE map of glioblastoma proteins. 2DE separation with following imaging, immunochemistry, spot picking, and mass-spectrometry allowed us detecting and identifying more than 100 proteins. Several of them have prominent differences in their level between norm and cancer. Among them are alpha-enolase (ENOA_HUMAN), pyruvate kinase isozymes M1/M2 (KPYM_HUMAN), cofilin 1 (COF1_HUMAN), translationally-controlled tumor protein TCTP_HUMAN, annexin 1 (ANXA1_HUMAN), PCNA (PCNA_HUMAN), p53 (TP53_HUMAN) and others. Most interesting results were obtained with protein p53. In all glioblastoma cell lines, its level was dramatically up regulated and enriched by multiple additional isoforms. This distribution is well correlated with presence of these proteins inside of cells themselves. At this initial step we suggest the panel of specific brain tumor markers (signature) to help creating noninvasive techniques to diagnose disease. These preliminary data point to these proteins as promising markers of glioblastoma.

scholarly journals Proteomic analysis of human glioblastoma cell lines differently resistant to a nitric oxide releasing agent

2015 ◽  
Vol 11 (6) ◽  
pp. 1612-1621 ◽  
Author(s):  
Roberta Leone ◽  
Paola Giussani ◽  
Sara De Palma ◽  
Chiara Fania ◽  
Daniele Capitanio ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Lines ◽  
Glioma Cell ◽  
High Grade Glioma ◽  
High Grade ◽  
Glioblastoma Cell ◽  
Proteomic Profile ◽  
Glioma Cell Lines ◽  
Nitric Oxide Releasing ◽  
Glioblastoma Cell Lines

NO exposure of two human high grade glioma cell lines (CCF-STTG1 and T98G) characterized by a different proteomic profile shows differential ceramide distribution and proliferation.

scholarly journals Smarcd1 Inhibits the Malignant Phenotypes of Human Glioblastoma Cells via Crosstalk with Notch1

2020 ◽  
Author(s):  
Yihao Zhu ◽  
Handong Wang ◽  
Maoxing Fei ◽  
Ting Tang ◽  
Wenhao Niu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Lines ◽  
High Grade Glioma ◽  
Glioblastoma Cell ◽  
Glioblastoma Cells ◽  
Human Glioblastoma ◽  
Protein Levels ◽  
Enhanced Expression ◽  
Human Glioblastoma Cells ◽  
Glioblastoma Cell Lines

AbstractSmarcd1 is a component of an evolutionary conserved chromatin remodeling complex—SWI/SNF, which is involved in transcription factor recruitment, DNA replication, recombination, and repair. Suppression of the SWI/SNF complex required for cellular differentiation and gene regulation may be inducible for cell proliferation and tumorigenicity. However, the inhibitory role of Smarcd1 in human glioblastoma cells has not been well illustrated. Both U87 and U251 human glioblastoma cell lines were employed in the present study. The lentivirus-mediated gene knockdown and overexpression approach was conducted to determine the function of Smarcd1. The protein levels were tested by western blot, and the relative mRNA contents were detected by quantitative real-time PCR. Cell viability was tested by CCK-8 and colony-forming assay. Transwell assays were utilized to evaluate the motility and invasive ability. Flow cytometry was employed to analyze cell cycle and apoptosis. SPSS software was used for statistical analysis. Low expression of Smarcd1 was observed in glioblastoma cell lines and in patients with high-grade glioma. Importantly, the depletion of Smarcd1 promoted cell proliferation, invasion, and chemoresistance, whereas enhanced expression of Smarcd1 inhibited tumor-malignant phenotypes. Mechanistic research demonstrated that overexpression of Smarcd1 decreased the expression of Notch1, while knockdown of Notch1 increased the expression of Smarcd1 through Hes1 suppression. Hence, the crosstalk between Smarcd1 and Notch1, which formed a feedback loop, was crucial in regulation of glioblastoma malignant phenotypes. Furthermore, targeting Smarcd1 could be a potential strategy for human glioblastoma treatment.

scholarly journals RDNA-14. RADIATION-INDUCED miR-4516 CONTRIBUTES TO RADIO-RESISTANCE AND PROMOTES AGGRESSIVE PHENOTYPE IN GLIOBLASTOMA

2019 ◽  
Vol 21 (Supplement_6) ◽  
pp. vi209-vi210
Author(s):  
Ebin Sebastian ◽  
Tiantian Cui ◽  
Erica Hlavin Bell ◽  
Joseph McElroy ◽  
Benjamin Johnson ◽  
...  
Keyword(s):  
Brain Tumor ◽  
Cell Viability ◽  
Cell Lines ◽  
Poor Prognosis ◽  
Radiation Treatment ◽  
Critical Role ◽  
Luciferase Reporter ◽  
Glioblastoma Cell ◽  
Clonogenic Assays ◽  
Glioblastoma Cell Lines

Abstract BACKGROUND Glioblastoma is the most aggressive brain tumor with poor prognosis despite the best available treatment. MicroRNAs (miRNAs) are emerging as promising, novel prognostic biomarkers and therapeutic targets in glioblastoma. In a previous study, we demonstrated that miR-4516 predicts poor prognosis and functions as an oncogene in glioblastoma. Aim of the current study is to examine the role miR-4516 in radiation resistance and identify downstream targets contributing to this phenotype METHODS Radiosensitization was evaluated by cell viability and clonogenic assays. Cell apoptosis was evaluated using flow cytometry and immunoblotting. Potential targets of miR-4516 were identified using bioinformatic analysis (Targetscan and miRDB) and confirmed by luciferase reporter assays. Results were validated using immunoblotting. miR-4516 expression in glioblastoma cell lines after radiation treatment was quantified by qRT-PCR. RESULTS Expression of miR-4516 was increased up to 15 fold following radiation treatment, peaking at around 15min-60 min in primary and established glioblastoma cell lines including GBM 08-387, GBM 30 and U87-MG. Furthermore, inhibition of miR-4516 sensitized GBM 08-387, GBM30 and U87-MG cells to radiation in comparison to control groups as determined by cell viability and clonogenic assays. Further, miR-4516 inhibition induced apoptosis in these cell lines following radiation treatment. While conducting mechanistic studies, we found that the tumor-promoting function of miR-4516 was, in part, mediated by inhibition of p21 and PTPN14, two direct targets of miR-4516 CONCLUSION Our data suggest that radiation induces the expression of miR-4516 in glioblastoma cell lines. This miRNA plays a critical role in radio-resistance and promotes aggressive phenotypes in glioblastoma and therefore, functional analyses of its target pathways may uncover novel therapeutically vulnerable target(s) in glioblastoma. FUNDING: R01CA108633, R01CA169368, RC2CA148190, U10CA180850-01(NCI), Brain Tumor Funders Collaborative Grant, and OSU-CCC (all to AC). The Ton and Patricia Bohnenn Fund for Neuro_Oncology Research (to PR).

scholarly journals AFM Observation of Heightened Cell Periphery of High-Grade Glioblastoma Cell Lines

2016 ◽  
Vol 6 (1) ◽  
pp. 47-53 ◽  
Author(s):  
James R. Smith ◽  
Zaynah Maherally ◽  
Samantha C. Higgins ◽  
Qian An ◽  
Helen L. Fillmore ◽  
...  
Keyword(s):  
Cell Lines ◽  
Cell Periphery ◽  
High Grade ◽  
Glioblastoma Cell ◽  
Afm Observation ◽  
Glioblastoma Cell Lines

scholarly journals Chemical composition of Polish propolis and its antiproliferative effect in combination with Bacopa monnieri on glioblastoma cell lines

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Justyna Moskwa ◽  
Sylwia K. Naliwajko ◽  
Renata Markiewicz-Żukowska ◽  
Krystyna J. Gromkowska-Kępka ◽  
Patryk Nowakowski ◽  
...  
Keyword(s):  
Mass Spectrometry ◽  
Chemical Composition ◽  
Cell Lines ◽  
Bacopa Monnieri ◽  
Gas Chromatography Mass Spectrometry ◽  
Array Detector ◽  
Proliferative Potential ◽  
Cytotoxicity Test ◽  
Glioblastoma Cell ◽  
Glioblastoma Cell Lines

AbstractPropolis and Bacopa monnieri (L.) Wettst. (Brahmi) are natural products that contain many active substances and possess anticancer properties. The aim of this study was to investigate the chemical composition of Polish propolis extract (PPE) by gas chromatography-mass spectrometry (GC–MS), B. monnieri extracts (BcH, BcS) by high performance liquid chromatography with diode array detector and mass spectrometry coupled with electrospray ionization (LC–ESI–MS) and finally determine its anti-proliferative potential combined with BcH and BcS in glioblastoma cell lines (T98G, LN-18, U87MG). The antiproliferative activity of PPE, BcH, BcS and their combination (PPE + BcH) was determined by a cytotoxicity test, and DNA binding was determined by [3H]-thymidine incorporation. Flavonoids and phenylpropenoids were the main components of PPE. BcH and BcS samples were also successfully analyzed. Their main constituents were saponins such as bacoside A3, bacopaside II, X and bacopasaponin C and its isomer. The inhibitory effects on the viability and proliferation of the tested glioma cells observed after incubation with the combination of PPE and BcH were significantly stronger than the effects of these two extracts separately. These findings suggest that propolis in combination with B. monnieri shows promising anticancer activity for the treatment of glioblastoma. However, further studies are still required.

scholarly journals Pediatric High Grade Glioma Resources From the Children’s Brain Tumor Tissue Consortium (CBTTC) and Pediatric Brain Tumor Atlas (PBTA)

2019 ◽  
Author(s):  
Heba Ijaz ◽  
Mateusz Koptyra ◽  
Krutika S. Gaonkar ◽  
Jo Lynne Rokita ◽  
Valerie P. Baubet ◽  
...  
Keyword(s):  
Brain Tumor ◽  
Cell Lines ◽  
Glioma Cell ◽  
Tumor Tissue ◽  
Pediatric Brain Tumor ◽  
High Grade Glioma ◽  
High Grade ◽  
Primary Tumors ◽  
Pediatric Brain ◽  
Pediatric High Grade Glioma

ABSTRACTBackgroundPediatric high grade glioma (pHGG) remains a fatal disease. Increased access to richly annotated biospecimens and patient derived tumor models will accelerate pHGG research and support translation of research discoveries. This work describes the pediatric high grade glioma set of the Children’s Brain Tumor Tissue Consortium (CBTTC) from the first release (October 2018) of the Pediatric Brain Tumor Atlas (PBTA).MethodspHGG tumors with associated clinical data and imaging were prospectively collected through the CBTTC and analyzed as the Pediatric Brain Tumor Atlas (PBTA) with processed genomic data deposited into PedcBioPortal for broad access and visualization. Matched tumor was cultured to create high grade glioma cell lines analyzed by targeted and WGS and RNA-seq. A tissue microarray (TMA) of primary pHGG tumors was also created.ResultsThe pHGG set included 87 collection events (73 patients, 60% at diagnosis, median age of 9 yrs, 55% female, 46% hemispheric). Analysis of somatic mutations and copy number alterations of known glioma genes were of expected distribution (36% H3.3, 47% TP53, 24% ATRX and 7% BRAF V600E variants). A pHGG TMA (n=77), includes 36 (53%) patient tumors with matched sequencing. At least one established glioma cell line was generated from 23 patients (32%). Unique reagents include those derived from a H3.3 G34R glioma and from tumors with mismatch repair deficiency.ConclusionThe CBTTC and PBTA have created an openly available integrated resource of over 2,000 tumors, including a rich set of pHGG primary tumors, corresponding cell lines and archival fixed tissue to advance translational research for pHGG.IMPORTANCE OF STUDYHigh-grade gliomas (HGG) remain the leading cause of cancer death in children. Since molecularly heterogeneous, preclinical studies of pediatric HGG will be most informative if able to compare across groups. Given their relatively rarity, there are few readily available biospecimens and cellular models to inform preclinical laboratory and genomic translational research. Therefore, the aim of this CBTTC study was to highlight the panel of pediatric HGG cases whose primary tumors have undergone extensive genomic analysis, have clinical data, available imaging and additional biospecimens, including tumor, nucleic acids, cell lines and FFPE tissue on a tissue microarray (TMA).

scholarly journals PDTM-16. PEDIATRIC HIGH GRADE GLIOMA RESOURCES FROM THE CHILDREN’S BRAIN TUMOR TISSUE CONSORTIUM (CBTTC) AND PEDIATRIC BRAIN TUMOR ATLAS (PBTA)

2019 ◽  
Vol 21 (Supplement_6) ◽  
pp. vi190-vi190
Author(s):  
Heba Ijaz ◽  
Mateusz Koptyra ◽  
Krutika Gaonkar ◽  
Jo Lynne Rokita ◽  
Valerie Baubet ◽  
...  
Keyword(s):  
Brain Tumor ◽  
Mismatch Repair ◽  
Cell Lines ◽  
Glioma Cell ◽  
Tumor Tissue ◽  
Pediatric Brain Tumor ◽  
High Grade Glioma ◽  
High Grade ◽  
Pediatric Brain ◽  
Pediatric High Grade Glioma

Abstract BACKGROUND Pediatric high grade glioma (pHGG) remains a fatal disease. Access to richly annotated biospecimens and patient derived tumor models will accelerate pHGG research and support translation of research discoveries. This work describes the pediatric high grade glioma set of the Children’s Brain Tumor Tissue Consortium (CBTTC) from the first release of the Pediatric Brain Tumor Atlas (PBTA). METHODS pHGG tumors with associated clinical data and imaging were prospectively collected through the CBTTC and analyzed as the Pediatric Brain Tumor Atlas (PBTA) with processed genomic data deposited into PedcBioPortal for broad access and visualization. Matched tumor was cultured to create high grade glioma cell lines analyzed by targeted and WGS and RNA-seq. A tissue microarray (TMA) of primary pHGG tumors was also created. RESULTS The pHGG set includes 87 collection events (73 patients, 60% at diagnosis, median age of 9 yrs, 55% female, 46% hemispheric). Operative reports, pathology reports and histology images are available for nearly all cases. Pre- and post-operative MRI images and reports are also available for a subset. Tumor WGS/RNAseq is available for 70 subjects. Analysis of somatic mutations and copy number alterations of known glioma genes were of expected distribution (36% H3.3, 47% TP53, 24% ATRX and 7% BRAFV600E variants). In our panel of pHGG, six patients (8 tumors) harbored germline mismatch repair mutations with tumor hyper-mutation. A pHGG TMA (n=77), includes 36 patient tumors with matched sequencing. At least one established glioma cell line was generated from 23 patients (32%). Unique reagents include those derived from a H3.3 G34R glioma and from tumors with mismatch repair deficiency. CONCLUSION The CBTTC and PBTA have created an openly available integrated resource of over 2,000 tumors, including a rich set of pHGG primary tumors, corresponding cell lines and archival fixed tissue to advance translational research for pHGG.

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