TATIANE KATSUE FURUYA
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Radiologia, Faculdade de Medicina
LIM/05 - Laboratório de Poluição Atmosférica Experimental, Hospital das Clínicas, Faculdade de Medicina
LIM/24 - Laboratório de Oncologia Experimental, Hospital das Clínicas, Faculdade de Medicina
LIM/05 - Laboratório de Poluição Atmosférica Experimental, Hospital das Clínicas, Faculdade de Medicina
LIM/24 - Laboratório de Oncologia Experimental, Hospital das Clínicas, Faculdade de Medicina
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bookPart Modulação da expressão gênica e epigenética(2022) SANTOS, Nathalia Leal; NAGAI, Maria Aparecida; FURUYA, Tatiane Katsue- deltaXpress (ΔXpress): a tool for mapping differentially correlated genes using single-cell qPCR data(2023) CARRASCO, Alexis German Murillo; FURUYA, Tatiane Katsue; UNO, Miyuki; JR, Tharcisio Citrangulo Tortelli; CHAMMAS, RogerBackgroundHigh-throughput experiments provide deep insight into the molecular biology of different species, but more tools need to be developed to handle this type of data. At the transcriptomics level, quantitative Polymerase Chain Reaction technology (qPCR) can be affordably adapted to produce high-throughput results through a single-cell approach. In addition to comparative expression profiles between groups, single-cell approaches allow us to evaluate and propose new dependency relationships among markers. However, this alternative has not been explored before for large-scale qPCR-based experiments.ResultsHerein, we present deltaXpress (Delta Xpress), a web app for analyzing data from single-cell qPCR experiments using a combination of HTML and R programming languages in a friendly environment. This application uses cycle threshold (Ct) values and categorical information for each sample as input, allowing the best pair of housekeeping genes to be chosen to normalize the expression of target genes. Delta Xpress emulates a bulk analysis by observing differentially expressed genes, but in addition, it allows the discovery of pairwise genes differentially correlated when comparing two experimental conditions. Researchers can download normalized data or use subsequent modules to map differentially correlated genes, perform conventional comparisons between experimental groups, obtain additional information about their genes (gene glossary), and generate ready-to-publication images (600 dots per inch).Conclusions Delta Xpress web app is freely available to non-commercial users at https://alexismurillo.shinyapps.io/dXpress/ and can be used for different experiments in all technologies involving qPCR with at least one housekeeping region.
- Good response to long-term therapy with growth hormone in a patient with 9p trisomy syndrome: A case report and review of the literature(2016) CANTON, Ana Pinheiro Machado; NISHI, Mirian Yumie; FURUYA, Tatiane Katsue; ROELA, Rosimeire Aparecida; JORGE, Alexander Augusto LimaThe 9p trisomy syndrome is a rare condition, clinically characterized by a wide range of dysmorphic features, intellectual disability, and, in most patients, by short stature. Recombinant human growth hormone (rhGH) therapy is still controversial in syndromic disorders, the reason for which it is not currently indicated. Here we report a 7-year-old boy with 9p trisomy syndrome and marked short stature. Results of routine laboratory assessments were normal. IGF1 and IGFBP3 levels were both in the normal range (-1.6 and -0.7 SDS, respectively). GH peak in response to oral clonidine stimulation test was 3.5g/L, which is considered a normal response. Chromosomal analysis revealed the karyotype 47,XY,+del(9)(pter-q11:) dn. SNP array data indicated absence of mosaicism [arr 9p24.3-p13.1 (203,861-38,787,480) x3]. By the age of 8.3 years, the patient had persistent short stature (-2.9 SDS) with normal growth velocity (4.9cm/y; -0.7 SDS), not showing spontaneous catch-up. After 5.6 years of rhGH therapy (50g/kg/d), height SDS improved from -2.9 to -1.0. This result suggests that rhGH therapy could be considered for patients with 9p trisomy syndrome who present with short stature. The degree of intellectual disability and the potential for social inclusion should be taken into account when recommending this treatment. Additional studies are needed to establish the benefits of height gain in these patients. (c) 2015 Wiley Periodicals, Inc.
- Allergic sensitization and exposure to ambient air pollution beginning early in life lead to a COPD-like phenotype in young adult mice(2022) COSTA, Natalia de Souza Xavier; TELES, Aila Mirtes; BRITO, Jose Mara de; LOPES, Thais de Barros Mendes; ROSSI, Renata Calciolari; MAGALHAES, Fernanda; COSTA, Arantes; SARAIVA-ROMANHOLO, Beatriz Mangueira; PERINI, Adenir; FURUYA, Tatiane Katsue; CARRASCO, Alexis German Murillo; VERAS, Mariana Matera; SALDIVA, Paulo Hilaroi Nascimento; CHAMMAS, Roger; MAUAD, ThaisThe perinatal period and early infancy are considered critical periods for lung development. During this period, adversities such as environmental exposures, allergic sensitization, and asthma are believed to impact lung health in adulthood. Therefore, we hypothesized that concomitant exposure to allergic sensitization and urban -derived fine particulate matter (PM2.5) in the early postnatal period of mice would cause more profound alter-ations in lung alveolarization and growth and differently modulate lung inflammation and gene expression than either insult alone in adult life. BALB/c mice were sensitized with ovalbumin (OVA) and exposed to PM2.5 from the fifth day of life. Then, we assessed lung responsiveness, inflammation in BALF, lung tissue, and alveolari-zation by stereology. In addition, we performed a transcriptomic analysis of lung tissue on the 40th day of life. Our results showed that young adult mice submitted to allergic sensitization and exposure to ambient PM2.5 since early life presented decreased lung growth with impaired alveolarization, a mixed neutrophilic-eosinophilic pattern of lung inflammation, increased airway responsiveness, and increased expression of genes linked to neutrophil recruitment when compared to animals that were OVA-sensitized or PM(2.5 )exposed only. Both, early life allergic sensitization and PM2.5 exposure, induced inflammation and impaired lung growth, but concomitant exposure was associated with worsened inflammation parameters and caused alveolar enlargement. Our experimental data provide pathological support for the hypothesis that allergic or environmental insults in early life have permanent adverse consequences for lung growth. In addition, combined insults were associated with the development of a COPD-like phenotype in young adult mice. Together with our data, current evidence points to the urgent need for healthier environments with fewer childhood disadvantage factors during the critical windows of lung development and growth.
- Cyclooxygenase-2 gene polymorphisms and susceptibility to colorectal cancer in a Brazilian population(2017) TOMITAO, Michele Tatiana Pereira; NAHAS, Sergio Carlos; KUBRUSLY, Marcia Saldanha; FURUYA, Tatiane Katsue; DINIZ, Marcio Augusto; MARIE, Suely Kazue Nagahashi; SAFATLE-RIBEIRO, Adriana Vaz; ELUF-NETO, Jose; CECCONELLO, Ivan; RIBEIRO JR., UlyssesBackground: Multi-ethnicity of Brazilian population displays high levels of genomic diversity. Polymorphism may detect people at higher risk of developing cancer, distinctive response to treatment, and prognosis. Cyclooxygenase-2 (COX-2) is induced in response to growth factors and cytokines, and is expressed in inflammatory diseases, precancerous lesions and colorectal cancer (CRC). The aim of this study was to evaluate the influence of COX-2 -1195A > G and 8473T > C polymorphisms as a risk factor of developing CRC. Methods: We evaluated COX-2 Single Nucleotide Polymorphism (SNP) of 230 CRC patients and 196 healthy controls by Real-Time Polymerase Chain Reaction. Results: Populations were in Hardy-Weinberg equilibrium (HWE), except for control group of 8473T > C SNP. The frequencies were similar in both groups for genotypes and haplotypes. There was no association between studied polymorphisms and risk of CRC. Conclusions: The gene polymorphisms studied do not participate in the genetic susceptibility to CRC in a Brazilian population.
- Disruption of miRNA-mRNA Networks Defines Novel Molecular Signatures for Penile Carcinogenesis(2021) FURUYA, Tatiane Katsue; MURTA, Claudio Bovolenta; CARRASCO, Alexis German Murillo; UNO, Miyuki; SICHERO, Laura; VILLA, Luisa Lina; CARDILLI, Leonardo; COELHO, Rafael Ferreira; GUGLIELMETTI, Giuliano Betoni; CORDEIRO, Mauricio Dener; LEITE, Katia Ramos Moreira; NAHAS, William Carlos; CHAMMAS, Roger; JR, Jose PontesSimple Summary: As there are still no biomarkers reported in clinical practice in penile cancer (PeC), we aimed to investigate and validate molecular signatures based on miRNA and mRNA profiles to identify molecular drivers and pathways involved in PeC tumorigenesis. We found eight DEmiRs and 37 DEGs comparing tumoral tissues (TT) paired with non-neoplastic tissues (NNT) of PeC patients. Four downregulated DEmiRs (miR-30a-5p, miR-432-5p, miR-487b-3p, and miR-145-5p) and six upregulated DEGs (IL1A, MCM2, MMP1, MMP12, SFN and VEGFA) were identified as potential biomarkers in PeC by their capacity of discriminating TT and NNT with accuracy. Furthermore, we performed an analysis of miRNA-mRNA interaction and found disruption in the dynamics of the regulation of eight pairs during tumor development that have never been described in PeC. Taken together, our findings contribute to a better understanding of the regulatory roles of miRNAs and altered transcripts levels in penile carcinogenesis. Penile cancer (PeC) carcinogenesis is not fully understood, and no biomarkers are reported in clinical practice. We aimed to investigate molecular signatures based on miRNA and mRNA and perform an integrative analysis to identify molecular drivers and pathways for PeC development. Affymetrix miRNA microarray was used to identify differentially expressed miRNAs (DEmiRs) comparing 11 tumoral tissues (TT) paired with non-neoplastic tissues (NNT) with further validation in an independent cohort (n = 13). We also investigated the mRNA expression of 83 genes in the total sample. Experimentally validated targets of DEmiRs, miRNA-mRNA networks, and enriched pathways were evaluated in silico. Eight out of 69 DEmiRs identified by microarray analysis were validated by qRT-PCR (miR-145-5p, miR-432-5p, miR-487b-3p, miR-30a-5p, miR-200a-5p, miR-224-5p, miR-31-3p and miR-31-5p). Furthermore, 37 differentially expressed genes (DEGs) were identified when comparing TT and NNT. We identified four downregulated DEmiRs (miR-30a-5p, miR-432-5p, miR-487b-3p, and miR-145-5p) and six upregulated DEGs (IL1A, MCM2, MMP1, MMP12, SFN and VEGFA) as potential biomarkers in PeC by their capacity of discriminating TT and NNT with accuracy. The integration analysis showed eight dysregulated miRNA-mRNA pairs in penile carcinogenesis. Taken together, our findings contribute to a better understanding of the regulatory roles of miRNAs and altered transcripts levels in penile carcinogenesis.
- Simultaneous silencing of lysophosphatidylcholine acyltransferases 1-4 by nucleic acid nanoparticles (NANPs) improves radiation response of melanoma cells(2021) SAITO, Renata F.; RANGEL, Maria Cristina; HALMAN, Justin R.; CHANDLER, Morgan; ANDRADE, Luciana Nogueira de Sousa; ODETE-BUSTOS, Silvina; FURUYA, Tatiane Katsue; CARRASCO, Alexis German Murillo; CHAVES-FILHO, Adriano B.; YOSHINAGA, Marcos Y.; MIYAMOTO, Sayuri; AFONIN, Kirill A.; CHAMMAS, RogerRadiation induces the generation of platelet-activating factor receptor (PAF-R) ligands, including PAF and oxidized phospholipids. Alternatively, PAF is also synthesized by the biosynthetic enzymes lysophosphatidylcholine acyltransferases (LPCATs) which are expressed by tumor cells including melanoma. The activation of PAF-R by PAF and oxidized lipids triggers a survival response protecting tumor cells from radiation-induced cell death, suggesting the involvement of the PAF/PAF-R axis in radioresistance. Here, we investigated the role of LPCATs in the melanoma cell radiotherapy response. LPCAT is a family of four enzymes, LPCAT1-4, and modular nucleic acid nanoparticles (NANPs) allowed for the simultaneous silencing of all four LPCATs. We found that the in vitro simultaneous silencing of all four LPCAT transcripts by NANPs enhanced the therapeutic effects of radiation in melanoma cells by increasing cell death, reducing long-term cell survival, and activating apoptosis. Thus, we propose that NANPs are an effective strategy for improving radiotherapy efficacy in melanomas.
- Extracellular Vesicles Shedding Promotes Melanoma Growth in Response to Chemotherapy(2019) ANDRADE, Luciana Nogueira de Sousa; OTAKE, Andreia Hanada; CARDIM, Silvia Guedes Braga; SILVA, Felipe I. Lelis da; SAKAMOTO, Mariana Mari Ikoma; FURUYA, Tatiane Katsue; UNO, Miyuki; PASINI, Fatima Solange; CHAMMAS, RogerExtracellular vesicles (EVs) are emerging as key players in intercellular communication. EVs can transfer biological macromolecules to recipient cells, modulating various physiological and pathological processes. It has been shown that tumor cells secrete large amounts of EVs that can be taken up by malignant and stromal cells, dictating tumor progression. In this study, we investigated whether EVs secreted by melanoma cells in response to chemotherapy modulate tumor response to alkylating drugs. Our findings showed that human and murine melanoma cells secrete more EVs after treatment with temozolomide and cisplatin. We observed that EVs shed by melanoma cells after temozolomide treatment modify macrophage phenotype by skewing macrophage activation towards the M2 phenotype through upregulation of M2-marker genes. Moreover, these EVs were able to favor melanoma re-growth in vivo, which was accompanied by an increase in Arginase 1 and IL10 gene expression levels by stromal cells and an increase in genes related to DNA repair, cell survival and stemness in tumor cells. Taken together, this study suggests that EVs shed by tumor cells in response to chemotherapy promote tumor repopulation and treatment failure through cellular reprogramming in melanoma cells.
- Correlation of microRNA expression profile and prognosis of penile cancer: A prospective study using microarray data analysis(2018) MURTA, Claudio Bovolenta; PONTES JR., Jose; FURUYA, Tatiane Katsue; UNO, Miyuki; CARRASCO, Alexis; SICHERO, Laura; VILLA, Luisa Lina; CORDEIRO, Mauricio; GUGLIELMETTI, Giuliano; COELHO, Rafael; LEITE, Katia Ramos Moreira; SROUGI, Miguel; CHAMMAS, Roger; NAHAS, William Carlos
- MicroRNA-195 acts as an anti-proliferative miRNA in human melanoma cells by targeting Prohibitin 1(2017) CIRILO, Priscila Daniele Ramos; ANDRADE, Luciana Nogueira de Sousa; CORREA, Bruna Renata Silva; QIAO, Mei; FURUYA, Tatiane Katsue; CHAMMAS, Roger; PENALVA, Luiz Otavio FerrazBackground: Melanoma is the most lethal type of skin cancer. Since chemoresistance is a significant barrier, identification of regulators affecting chemosensitivity is necessary in order to create new forms of intervention. Prohibitin 1 (PHB1) can act as anti-apoptotic or tumor suppressor molecule, depending on its subcellular localization. Our recent data shown that accumulation of PHB1 protects melanoma cells from chemotherapy-induced cell death. Lacking of post-transcriptional regulation of PHB1 could explain this accumulation. Interestingly, most of melanoma patients have down-regulation of microRNA-195. Here, we investigate the role of miR-195, its impact on PHB1 expression, and on chemosensitivity in melanoma cells. Methods: TCGA-RNAseq data obtained from 341 melanoma patient samples as well as a panel of melanoma cell lines were used in an expression correlation analysis between PHB1 and predicted miRNAs. miR-195 impact on PHB1 mRNA and protein levels and relevance of this regulation were investigated in UACC-62 and SK-MEL-5 melanoma lines by RT-qPCR and western blot, luciferase reporter and genetic rescue experiments. Cell proliferation, cell-cycle analysis and caspase 3/7 assay were performed to investigate the potential action of miR-195 as chemosensitizer in melanoma cells treated with cisplatin and temozolomide. Results: Analysis of the TCGA-RNAseq revealed a significant negative correlation (Pearson) between miR-195 and PHB1 expression. Moreover, RT-qPCR data showed that miR-195 is down-regulated while PHB1 is up-regulated in a collection of melanoma cells. We demonstrated that miR-195 regulates PHB1 directly by RT-qPCR and western blot in melanoma cells and luciferase assays. To establish PHB1 as a relevant target of miR-195, we conducted rescue experiments in which we showed that PHB1 transgenic expression could antagonize the suppressive effect miR-195 on the proliferation of melanoma cells. Finally, transfection experiments combined with drug treatments performed in the UACC-62 and SK-MEL-5 melanoma cells corroborated miR-195 as potential anti-proliferative agent, with potential impact in sensitization of melanoma cell death. Conclusions: This study support the role of miR-195 as anti-proliferative miRNA via targeting of PHB1 in melanoma cells.