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  • 1
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    Abstract 3739: Understanding the link between glutamine metabolism and angiogenesis in astrocytoma
    American Association for Cancer Research (AACR) ; 2020
    In:  Cancer Research Vol. 80, No. 16_Supplement ( 2020-08-15), p. 3739-3739
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 80, No. 16_Supplement ( 2020-08-15), p. 3739-3739
    Abstract: Angiogenic switch is a hallmark for tumor growth, and strategies to inhibit this process have been pursued for cancer therapy, but with limited long-term efficacy. Recently, targeting endothelial cell (EC) metabolism emerged as an alternative to regulate angiogenesis. In fact, glutamine metabolism is essential for EC sprouting in vitro, and the consumption/secretion rate measurements revealed that proliferating ECs consumed glutamine more than any other amino acid. Glutamine is transported into the cells and converted into α-ketoglutarate to enter the tricarboxylic acid cycle through glutaminolysis, which is upregulated in cancer. Glutaminase (coded by GLS), the main regulator of this pathway, presents two isoforms: GLSiso1 and GLSiso2. We have analyzed the expression level of both GLS isoforms in different grades of astrocytoma, with a gradual increase of their expressions in parallel to the malignancy. GLSiso1 was highly expressed in normal brain samples, in contrast to low GLSiso2 expression, indicating GLSiso2 as a more eligible therapeutic target. GLSiso2-specific transcript inhibition by siRNA in GBM U87MG cells lead to significant decrease of tumor cell proliferation, and a temozolomide-sensitizing effect, relative to NTC-controls. The RNASeq transcriptome analysis of these GLSiso2-silenced cells revealed a differential expression of genes related to blood vessel development, extracellular matrix organization, angiogenesis and tube development with FDR of 4.95e-04, 5.25e-06, 5.92e-05, 8.6e-06 and 1.0e-04, respectively. The immunohistochemistry analysis in human astrocytoma FFPE samples demonstrated GLS positivity on tumor cells and blood vessels, with higher protein expression in more malignant astrocytoma. Such observation corroborated the transcriptomic finding of GLSiso2 participation in the EC compartment. Moreover, the system biology analysis revealed an interesting net among GLS, TP53, ITB1, TGFBI, TGFBR1/2, COL1A1/2, COL5A2, LUM, ENG, ANGPT1 connecting genes related to metabolism, extracellular matrix and angiogenesis. In the search for the most suitable EC line to study the impact of GLS isoforms on the vessel compartment, we observed that HUVEC immortalized umbilical EC line presented higher expression of GLSiso2 than GLSiso1. Chemical blockade of the total GLS by BPTES and 968 was tested in HUVEC cells and a significant proliferation and migration decrease were observed. Further GLSiso2 specific silencing of ECs might clarify the crosstalk between tumor cells and ECs, and will allow the identification of key targets in their metabolic reprogramming during tumor growth. Citation Format: Yollanda E. Franco, Roseli S. Soares, Marina T. Lima, Antonio M. Lerario, Sueli M. Shinjo, Suely K. Marie. Understanding the link between glutamine metabolism and angiogenesis in astrocytoma [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 3739.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2020-3739
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
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  • 2
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    Abstract 2958: Transcriptome analysis of astrocytoma versus non-neoplastic human microglia
    American Association for Cancer Research (AACR) ; 2017
    In:  Cancer Research Vol. 77, No. 13_Supplement ( 2017-07-01), p. 2958-2958
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 77, No. 13_Supplement ( 2017-07-01), p. 2958-2958
    Abstract: Diffuse gliomas are primary brain tumors characterized by infiltrative growth and high heterogeneity, rendering the disease mostly incurable. Advances in genetic analysis revealed that molecular alterations predict patients’ overall survival and clinical outcome. However, glioma tumorigenicity is not exclusively caused by its genetic alterations. The crosstalk between tumor cells and the surrounding microenvironment plays a crucial role in modulating glioma growth and aggressiveness. The most abundant non-neoplastic cells in this microenvironment belong to the myeloid lineage, comprising CNS-resident microglia and infiltrating monocytes/macrophages (iTAMs). Understanding the dynamics between tumor and myeloid cells and the changes leading to pro-tumorigenic activation of innate immunity cells would elucidate potential treatment alternatives. Microglia were isolated from the parietal cortex of 16 autopsy samples of cognitively intact humans (non-neoplastic, NN) and from 6 glioma samples (three GBMs, one anaplastic astrocytoma and two low grade astrocytoma, TU-glia), and their mRNA expression profile was determined by deep sequencing. The comparison of these transcriptome datasets provided an incomparable landscape of the crosstalk between immune and tumor cells. Our preliminary analysis shows that differences between NN microglia and TU-uglia go beyond inflammation specific genes. While there is overexpression of anti-inflammatory markers (CD163, IL2RA, CXCL2 and TGFB1), implying pro-tumorigenic characteristics, there is also high expression of genes indicative of an acute, pro-inflammatory response, such as IL1B, CCL5, CCR7 and TNFA. Further analysis showed that TU-uglia expressed high levels of genes related to extracellular matrix (ECM) remodeling, such as fibronectin (FN1) and tenascin-C (TNC), as well as their ligands (ITGA4 and ITGB1), indicating that microglia, and not tumor cells, might be the main source for those proteins in the tumor microenvironment. We were also able to collect one sample of iTAMs from a GBM case. Despite not providing a significant number for statistical analysis, we can already see major differences in gene expression between this sample and our TU-uglia cohort. We identified surface receptors differentially expressed between both cell types (i.e.: ROBO1 and PDGFRA for TU-uglia, MARCO and MET for iTAMs), as well as transcription factors associated with stemness and proliferation, such as KLF4, SOX2 and OCT4 (the last two exclusive for TU-uglia). These results demonstrate that different activation signaling pathways occur within the same tumor sample. Microglia and iTAMs are subject to a number of signals from different clones of tumor cells, driving different responses along the progression of the disease, increasing its tumorigenicity. Better knowledge of this dynamics will help improve our understanding of gliomas and alternative treatment options. Citation Format: Thais Fernanda Galatro, Antonio M. Lerario, Sueli M. Oba-Shinjo, Bart J. Eggen, Suely K. Marie. Transcriptome analysis of astrocytoma versus non-neoplastic human microglia [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 2958. doi:10.1158/1538-7445.AM2017-2958
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2017-2958
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2017
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  • 3
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    Abstract 899: CD99 plays an important role in glioblastoma cell migration
    American Association for Cancer Research (AACR) ; 2017
    In:  Cancer Research Vol. 77, No. 13_Supplement ( 2017-07-01), p. 899-899
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 77, No. 13_Supplement ( 2017-07-01), p. 899-899
    Abstract: Glioblastoma (GBM) is the most common and aggressive malignant brain tumor in adults and the standard treatment consists of surgical resection of the tumor followed by radiation and chemotherapy with temozolomide. A combination of standard therapy with other biologically-based therapies is necessary to improve the survival of patients with GBM, which currently stands only to 15-17 months. In this sense many studies have been developed in pursuit of expressed membrane proteins in GBM, which are potential targets for immunotherapy. Our laboratory demonstrated increased CD99 mRNA and protein expression in GBM samples. CD99 has a key role in several biological processes, including cell adhesion, migration, apoptosis, differentiation of T cells and thymocytes, diapedesis of lymphocytes to inflamed vascular endothelium, maintenance of cellular morphology and regulation of intracellular membrane protein trafficking. In this study, the transcriptome of two GBM cell lines (U87MG and A172) transfected with siRNA for CD99 were analyzed in relation to the non-target control (NTC). A total of 728 genes (hypoexpressed with fold change ≤-1.5 relative to NTC or hyperexpressed with fold change ≥1.5 relative to NTC) were observed in both cell lines. An enrichment analysis by MetaCoreTM revealed the following processes as the most significant: (1) Cytoskeleton_Regulation of cytoskeleton rearrangement, (2) Cell adhesion_Cell-matrix interactions (3) Development_Blood vessel morphogenesis. Further, both cell lines were silenced for CD99 expression by shRNA (two clones) to perform functional assays, as wound healing (migration assay), adhesion, invasion and apoptosis. The CD99 knockdown reduced migration in both cell lines, with the highest decrease of the migration observed in the highest CD99 knockdown. Adhesion assay was performed using fibronectin as an extracellular matrix substrate. U87MG cells showed greater adhesion to fibronectin than the control (scrambled shRNA). On the other hand, A172 cells knocked down for CD99 presented lower adherence to fibronectin than the control. Apoptosis analysis with shCD99 U87MG cells showed a tendency of cells entering into late apoptosis when treated with temozolamide for 48 hours, but the same was not observed in shCD99 A172 cells. Additionally, CD99 (RPE) and phaloidin (Alexa Fluor 488) colocalized at lamellipodia, suggesting that CD99 is related to cytoskeleton rearrangement in both GBM cell lines. The different phenotypic behavior of migration and apoptosis observed in these two GBM cell lines with different somatic mutation background may be due to distinct signaling activation. Migration/invasion is the major characteristics of GBM which limits the surgical tumor resection, and consequently leads to tumor recurrence. Therefore, further analysis of CD99 activating pathways in the context of cell migration is worthwhile to unveil new therapeutic strategies to halt GBM progression. Citation Format: Lais C. Cardoso, Antonio M. Lerario, Suely K. Marie, Roseli S. Soares, Sueli M. Oba-Shinjo. CD99 plays an important role in glioblastoma cell migration [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 899. doi:10.1158/1538-7445.AM2017-899
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2017-899
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2017
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  • 4
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    Abstract 5378: Whole exome and RNA sequencing identify novel somatic mutations in gangliogliomas
    American Association for Cancer Research (AACR) ; 2018
    In:  Cancer Research Vol. 78, No. 13_Supplement ( 2018-07-01), p. 5378-5378
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 78, No. 13_Supplement ( 2018-07-01), p. 5378-5378
    Abstract: Gangliogliomas (GG) are rare, well differentiated, slow growing neuroepithelial tumors, composed of neoplastic mature ganglion cells and neoplastic glial cells. GG comprises 0.4% of all CNS primary tumors, and 70% of GG cases are diagnosed in patients with long-term temporal lobe epilepsy. The molecular pathogenesis of GG is poorly understood. Few groups have described a high frequency of a hotspot BRAF p.V600E mutation. More recently, a co-occurrence of histone H3 p.K27M and BRAF p.V600E mutations was reported in a pediatric midline grade I GG. However, the rarity of these tumors poses challenges to uncovering a more comprehensive landscape of somatic alterations. In this study, we describe the somatic mutational profiles of 12 GG from the University of Sao Paulo Medical School in one of the largest GG case series reported to date. We performed paired germline and somatic whole exome sequencing (WES) and RNA-Seq in all cases: 9 males and 3 females with ages ranging from 1 to 49 years (mean 17 ± 13 years). These tumors were located in the temporal lobe (8), frontal lobe (1), occipital lobe (1), intraventricular region (1), and intramedullary region (1). We used the Nextera Exome Enrichment Kit (Illumina) to perform WES, and the TruSeq Stranded Total RNA (Illumina) to perform RNA-Seq. Sequencing was performed in the Illumina HiSeq 2000. We aligned reads from WES and RNA-Seq libraries to the reference genome (hg19) using BWA and STAR, respectively. We used freebayes to perform variant call from germline WES paired with the respective tumor library (WES or RNA-Seq). We used the vcfcompare tool from vcflib to filter out germline variants and annovar to annotate the final list of variants. We identified mutations in cancer-related genes in 6/12 GGs: hotspot BRAF p.V600E in 4/6 cases, biallelic NF1 mutations (p.Y333X/p.R2258X) co-occurring with hotspot H3F3A (p.K27M) and FGFR1 (p.N546K) mutations in a 13-yo female with intraventricular GG, and, finally, biallelic hotspot TP53 mutations (p.V173M, p.P172T) combined with a hotspot IDH1 (p.R132H) mutation in a 26-yo male with frontal GG. Interestingly, the same combination of mutations observed in one of our patients (FGFR1 p.N546K/H3F3A p.K27M) was recently described in a diffuse leptomeningeal tumor with glial and neuronal markers. In summary, we identified novel mutations in cancer-related genes in 6 GG (50% of our cohort), including cases with mutations in more than one known cancer driver gene. In one of the largest GG case series reported to date, this study expands the spectrum of somatic alterations in GGs to include mutations in genes recurrently altered in higher-grade gliomas, such as IDH1, NF1, and TP53. Citation Format: Suely K. Marie, Sueli M. Oba-Shinjo, Antonio M. Lerario. Whole exome and RNA sequencing identify novel somatic mutations in gangliogliomas [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 5378.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2018-5378
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2018
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  • 5
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    Abstract 1501: Epigenetic dedifferentiation as a therapeutic strategy in adrenal cancer
    American Association for Cancer Research (AACR) ; 2023
    In:  Cancer Research Vol. 83, No. 7_Supplement ( 2023-04-04), p. 1501-1501
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 83, No. 7_Supplement ( 2023-04-04), p. 1501-1501
    Abstract: Adrenocortical carcinoma (ACC) is a rare cancer of the adrenal cortex without curative medical therapies. CIMP-high is an aggressive ACC molecular subtype defined by global CpG island hypermethylation with paradoxical activation of adrenal differentiation (driven by master transcription factor SF1) and stemness (driven by β-catenin). We show DNA hypermethylation redistributes histone methyltransferase EZH2 and its mark, H3K27me3. EZH2 inhibition remains lethal to CIMP-high ACC cells, erasing transcriptional programs without altering DNA methylation. We reconcile this phenomenon by discovery of two nuclear complexes, SF1/β-catenin and EZH2/β-catenin, present in physiology and persistent through advanced ACC. We find SF1/β-catenin is a chromatin-bound complex that controls the ACC super-enhancer landscape, while EZH2/β-catenin is restricted to off-chromatin pools. EZH2 inhibition purges SF1/β-catenin from chromatin, sparing EZH2/β-catenin, inducing dedifferentiation and restraining ACC growth in vitro and in vivo. Our studies illustrate how cell-of-origin programs dictate cancer evolution, exposing differentiation as an therapeutic vulnerability. Citation Format: Dipika R. Mohan, Kleiton S. Borges, Isabella Finco, Christopher R. LaPensee, Juilee Rege, Donald W. Little, Tobias Else, Madson Q. Almeida, Derek Dang, James Haggerty-Skeans, Ana Claudia Latronico, Berenice B. Mendonca, Richard J. Auchus, William E. Rainey, Suely K. Marie, Thomas J. Giordano, Sriram Venneti, Maria Candida B. Fragoso, David T. Breault, Antonio M. Lerario, Gary D. Hammer. Epigenetic dedifferentiation as a therapeutic strategy in adrenal cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 1501.
    Type of Medium: Online Resource
    ISSN: 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2023-1501
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2023
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  • 6
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    Abstract 2605: LOXL3 knock out affects pathways which involve cytoskeleton regulation, proliferation and apoptosis in glioblastoma cells
    American Association for Cancer Research (AACR) ; 2023
    In:  Cancer Research Vol. 83, No. 7_Supplement ( 2023-04-04), p. 2605-2605
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 83, No. 7_Supplement ( 2023-04-04), p. 2605-2605
    Abstract: Lysyl oxidase-like 3 (LOXL3), belonging to the lysyl oxidase family of copper-dependent amino oxidase, is responsible for the crosslinking of collagen and elastin. In tumors, the presence of LOXL3 has been associated with genomic stability, cell proliferation, and metastasis. In silico analysis has shown that glioblastoma was among the tumors with the highest LOXL3 expression levels. Moreover, LOXL3 expression increased with malignancy grade amongst diffusely infiltrative astrocytomas (from grade 2 to 4). In the present work, CRISPR-Cas9 gene editing was used to knock out LOXL3 in the human glioma U87MG cell line to evaluate the role of LOXL3 in glioblastoma. Analyses of protein expression level and genomic mutation mediated by CRISPR-Cas9 by two different sgRNA (denominated sgRNA1 and 2) were performed and the knock out efficiency and genome editing were confirmed. Transcriptome analysis of these cells revealed a downregulation of genes that coded for proteins involved in microtubule organization, cell division, and vesicle trafficking. On the other hand, upregulated genes when LOXL3 was knocked out in U87MG cells were involved in actin cytoskeleton, negative regulation of gene transcription, including chromatin remodeling, and cell-cell adhesion. Functional in vitro assays showed that LOXL3 knocked out cells presented decreased cell proliferation due to longer cell cycles with increased G1 and G2/M checkpoints compared to control cells. Additionally, LOXL3 knocked out U87MG cells presented a higher percentage of cells in the early phase of apoptosis with an increment after temozolomide treatment. Our results suggest an important role of LOXL3 in glioblastoma possibly mediated by cytoskeleton regulation, affecting cell proliferation, cell cycle, and cell death. These results reinforced the importance of LOXL3 in tumors, especially in glioblastoma, highlighting it as a potential therapeutic target. Citation Format: Talita S. Laurentino, Roseli S. Soares, Antonio M. Lerario, Suely K. Marie, Sueli Mieko Oba-Shinjo. LOXL3 knock out affects pathways which involve cytoskeleton regulation, proliferation and apoptosis in glioblastoma cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 2605.
    Type of Medium: Online Resource
    ISSN: 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2023-2605
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2023
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  • 7
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    Abstract 2596: Toll like receptor 4 as a potential DNA repair modulator in U87MG-GBM cells
    American Association for Cancer Research (AACR) ; 2020
    In:  Cancer Research Vol. 80, No. 16_Supplement ( 2020-08-15), p. 2596-2596
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 80, No. 16_Supplement ( 2020-08-15), p. 2596-2596
    Abstract: Toll like receptor 4 (TLR4) has a dual role in cellular fate, depending on the stimuli and microenvironment context. Its activation may promotes cell survival and proliferative phenotype via MyD88 with NFkB activation, or leads to cell death via TRIF. Glioblastoma (GBM), grade IV astrocytoma, is the most common and aggressive primary malignancy in the brain. Surgical tumor cytoreduction followed by radiotherapy and adjunct chemotherapy with Temozolomide (TMZ) have been considered the standard of care for GBM. And, in spite of several combinatory rescue therapeutic trials, the median overall survival of GBM patients continue to be approximately 15 months. In this context, new therapeutic strategies are urgent, and immune modulation has demonstrated optimistic results in several tumor types. Therefore, the aim of this study was to analyze the role of TLR4 in human astrocytomas. First, we evaluated TLR4 expression in 140 human astrocytoma of different grades of malignancy, by qRT-PCR. TLR4 molecular signaling pathways were investigated through LPS stimuli in U87MG-GBM cell line. In astrocytoma samples, TLR4 was up-regulated when compared to brain non-neoplastic samples (p & lt;0.05, Kruskall Wallis and Dunn tests), with increased expression in Mesenchymal compare to Classical and Proneural subtypes. U87MG cells stimulation with LPS (10ug/ml) lead to NF-kB (p65) nuclear translocation after 12hr through western blot and immunofluorescence, which was unexpected as such translocation through the MyD88/TRAF6 canonical pathway occurs within 30min to 2hr after LPS stimulation. TRIF, IL1B, RIPK1/3 expressions were increased after LPS stimulation, suggesting an activation of inflammasome and ripoptosome pathways. Moreover, the combined LPS treatment with TMZ showed a higher apoptotic rate after 48hr when compared to TMZ alone. However, the transcriptomic analysis by RNASeq of U87MG cells after LPS stimulation showed an upregulation of DNA repair genes, particularly MBD4 and PLAUR. Both genes are upregulated in mesenchymal GBM subtype in the TCGA RNASeq dataset, and they present correlated expression with TLR4 (r=0.406, p=0.004 and r=0.338, p=0.019 by Spearman's test). Our results suggest that the anti-tumoral effect by TLR4 pathway activation by enhancement of tumor apoptosis might be more efficient with combined inhibition of DNA repair cascade. In fact, OSI-296 and BKM-120 have shown to decrease MBD4 expression, and increased overall survival was observed in a phase II clinical trial for solid tumor. Citation Format: Isabele F. Moretti, Antonio Lerario, Sueli M. Oba-Shinjo, Suely K. Marie, Marina Trombetta Lima. Toll like receptor 4 as a potential DNA repair modulator in U87MG-GBM cells [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 2596.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2020-2596
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
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