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Pesquisa : A11.251.210.190 [Categoria DeCS]
Referências encontradas : 299 [refinar]
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Id: biblio-950882
Autor: Pan, Cuicui; Gao, Hua; Zheng, Ni; Gao, Qi; Si, Yuanquan; Zhao, Yueran.
Título: MiR-320 inhibits the growth of glioma cells through downregulating PBX3
Fonte: Biol. Res;50:31, 2017. graf.
Idioma: en.
Resumo: BACKGROUND: MiR-320 is downregulated in multiple cancers, including glioma and acts as tumor suppressor through inhibiting tumor cells proliferation and inducing apoptosis. PBX3 (Pre-B cell leukemia homeobox 3), a putative target gene of miR-320, has been reported to be upregulated in various tumors and promote tumor cell growth through regulating MAKP/ERK pathway. This study aimed to verify whether miR-320 influences glioma cells growth through regulating PBX3. METHODS: Twenty-four human glioma and paired adjacent nontumorous tissues were collected for determination of miR-320 and PBX3 expression using RT-qPCR and western blot assays. Luciferase reporter assay was performed to verify the interaction between miR-320 and its targeting sequence in the 3' UTR of PBX3 in glioma cells U87 and U251. Increased miR-320 level in U87 and U251 cells was achieved through miR-320 mimic transfection and the effect of which on glioma cells growth, proliferation, cell cycle, apoptosis and activation of Raf-1/MAPK pathway was determined using MTT, colony formation, flow cytometry and western blot assays. PBX3 knockdown was performed using shPBX3 and the influence on MAPK pathway activation was evaluated. RESULTS: MiR-320 downregulation and PBX3 upregulation was found in glioma tissues. Luciferase reporter assays identified miR-320 directly blinds to the 3' UTR of PBX3 in glioma cells. MiR-320 mimic transfection suppressed glioma cells proliferation, and induced cell cycle arrest and apoptosis. Both miR-320 overexpression and PBX3 knockdown inhibited Raf-1/MAPK activation. CONCLUSION: MiR-320 may suppress glioma cells growth and induced apoptosis through the PBX3/Raf-1/MAPK axis, and miR-320 oligonucleotides may be a potential cancer therapeutic for glioma.
Descritores: Neoplasias Encefálicas/metabolismo
Proteínas Proto-Oncogênicas/metabolismo
Proteínas de Homeodomínio/metabolismo
MicroRNAs/metabolismo
Glioma/metabolismo
-Neoplasias Encefálicas/patologia
Regulação para Baixo
Regulação Neoplásica da Expressão Gênica
Diferenciação Celular/efeitos dos fármacos
Regulação para Cima
Linhagem Celular Tumoral
Proliferação de Células/efeitos dos fármacos
Glioma/patologia
Limites: Humanos
Responsável: CL1.1 - Biblioteca Central


  2 / 299 LILACS  
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Id: biblio-950884
Autor: Du, Maotao; Zhang, Zhong; Gao, Tao.
Título: Piceatannol induced apoptosis through up-regulation of microRNA-181a in melanoma cells
Fonte: Biol. Res;50:36, 2017. graf.
Idioma: en.
Resumo: BACKGROUND: Melanoma took top position among the lethal cancers and, despite there have been some great attempts made to increase the natural life of patients with metastatic disease, long-lasting and complete remissions are few. Piceatannol, owns the similar function as resveratrol, has been defined as an anti-cancer agent playing important role in inhibition of proliferation, migration and metastasis in various cancer. Thus, we aim to investigate the anti-cancer effect and mechanisms of piceatannol in melanoma cells. METHODS: Melanoma cell lines WM266-4 and A2058 were treated either with or without piceatannol. Cell viability and cell apoptosis were assessed by using MTT and Annexin V/PI assay, respectively. Cells were transfected with specific miRNA using Lipfectamine 2000. miRNA bingding ability to 3'-UTR region within specific gene was assed by firefly luciferase analysis. Gene and protein expression was eveluated by qRT-PCR and western blot analysis, respectively. RESULTS: Our study showed that piceatannol inhibited WM266-4 and A2058 cells growth and induced apoptosis. Totally, 16 differentially expressed miRNAs were screened out including 8 up-regulated and 8 down-regulated miRNAs. Expression level of miR-181a is significantly higher in piceatannol-treated cells than normal control and is lower in melanoma cancer tissues than its adjacent normal tissues. Bcl-2 is a target gene of miR-181a. Moreover, silencing of miR-181a reverses the decrease of cell viability induced by piceatannol in WM266-4 and A2058 cells. Taken together, present study uncovered the ability of piceatannol to repress melanoma cell growth and clarified the contribution of miR-181a in the anticancer role of piceatannol. CONCLUSION: The present study proposes that piceatannol can be taken into account to be a hopeful anticancer agent for melanoma.
Descritores: Estilbenos/farmacologia
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Anticarcinógenos/farmacologia
Apoptose/efeitos dos fármacos
MicroRNAs/efeitos dos fármacos
Melanoma/tratamento farmacológico
-Regulação para Cima
Sobrevivência Celular
MicroRNAs/metabolismo
Linhagem Celular Tumoral
Melanoma/metabolismo
Melanoma/patologia
Limites: Humanos
Responsável: CL1.1 - Biblioteca Central


  3 / 299 LILACS  
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Id: biblio-950889
Autor: Agrawal, Sweta; Chaugule, Sachin; More, Shashank; Rane, Gargi; Indap, Madhavi.
Título: Methanolic extract of Euchelus asper exhibits in-ovo anti-angiogenic and in vitro anti-proliferative activities
Fonte: Biol. Res;50:41, 2017. tab, graf.
Idioma: en.
Projeto: University Grants Commission.
Resumo: BACKGROUND: The marine environment is a rich source of bioactive natural products. Many of the marine bioactive compounds have been derived successfully from molluscs. Euchelus asper is a marine mollusc which is commonly found in the intertidal rocky regions of the Mumbai coast. The present study was focused on evaluating the anti-angiogenic and anti- proliferative activities of methanolic extract of Euchelus asper (EAME). METHODS: The anti-angiogenic activity of EAME (50-800 µg/mL) was assessed by chick chorio-allantoic membrane (CAM) model wherein multiple parameters in the CAM blood vessels were analysed through morphometric and histo-logical investigations. In vitro testing of EAME (5-20 µg/mL) included its cytotoxicity against three different cancer cell lines, its effect on cell proliferation by wound healing assay as well as their relevant molecular mechanisms. Statistical analysis was carried out by two-tailed student's t test for two unpaired groups. RESULTS: Analysis of CAM revealed that the extract is effective in reducing the branching points of the 1st order blood vessels or capillaries of CAM. Histological analysis of CAM showed significant decrease in capillary plexus and compartmentalization along with increase in mesodermal blood vessels, thus establishing its anti-angiogenicity. Further, EAME exhibited moderate but significant cytotoxicity against A549 non-small cell lung carcinoma cell line. We also demonstrated that the cytotoxicity of EAME in A549 was associated with its apoptotic activity by subG1 phase arrest. Lastly, EAME significantly reduced A549 proliferation by reducing the expression of Matrix metalloproteinase-2 (MMP-2) and Matrix metalloproteinase-9 (MMP-9). CONCLUSION: Overall, our study suggested that EAME has potential to inhibit tumour angiogenic and proliferative activity and may be a potential source for development of new anti-cancer pharmaceuticals.
Descritores: Produtos Biológicos/farmacologia
Inibidores da Angiogênese/farmacologia
Proliferação de Células/efeitos dos fármacos
Gastrópodes/química
-Produtos Biológicos/isolamento & purificação
Inibidores da Angiogênese/isolamento & purificação
Linhagem Celular Tumoral/efeitos dos fármacos
Limites: Animais
Embrião de Galinha
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-950897
Autor: Li, Yu; Zhang, Depeng; Yu, Kaikai; Hu, Yudong; Wu, Qiong; Qian, Feng; Wang, Zishu.
Título: CMPD1 inhibited human gastric cancer cell proliferation by inducing apoptosis and G2/M cell cycle arrest
Fonte: Biol. Res;51:11, 2018. graf.
Idioma: en.
Projeto: Natural Science Foundation of Anhui Province (CN).
Resumo: BACKGROUND: Gastric cancer occupies the fourth highest morbidity rate of cancers worldwide. Clinical therapies of gastric cancer remain limited because of uncertainty of mechanisms and shortness of effective medicine. Thus, new drug candidates for gastric cancer treatment is urgently needed. RESULTS: In this study, CMPD1 as a wildly used MK2 phosphorylation inhibitor was employed to find its impact on gastric cancer cell proliferation, apoptosis and cell cycle using colony formation assay and flow cytometry analysis. Along with its anti-proliferation effect on gastric cancer cell line MKN-45 and SGC7901, CMPD1 also induced massive apoptosis and significant G2/M phase arrest in a time-dependent and dose-dependent manner in MKN-45 cells respectively. Furthermore, Western blot confirmed that the expression of anti-apoptotic proteins Bcl-2 was decreased while BAX, cytochrome c release and cleaved PARP were increased. In addition, oncogene c-Myc was downregulated in response to CMPD1 treatment. CONCLUSIONS: Our results demonstrated that CMPD1 has anti-tumor effect on human gastric cancer cell line MKN- 45 possibly via downregulating oncogene c-Myc expression and CMPD1 could be applied as a potential candidate for treating gastric malignancy. To the best of our knowledge, it is the first report of anti-tumor effect of CMPD-1 on human gastric cancer cells.
Descritores: Neoplasias Gástricas/tratamento farmacológico
Proteínas Serina-Treonina Quinases/farmacologia
Apoptose/efeitos dos fármacos
Peptídeos e Proteínas de Sinalização Intracelular/farmacologia
Proliferação de Células/efeitos dos fármacos
Fatores de Transcrição SOX9/farmacologia
Pontos de Checagem da Fase G2 do Ciclo Celular/efeitos dos fármacos
Antineoplásicos/farmacologia
-Neoplasias Gástricas/patologia
Regulação para Baixo/efeitos dos fármacos
Regulação para Cima/efeitos dos fármacos
Western Blotting
Reprodutibilidade dos Testes
Citocromos/efeitos dos fármacos
Linhagem Celular Tumoral
Proteínas Reguladoras de Apoptose/farmacologia
Citometria de Fluxo/métodos
Limites: Humanos
Tipo de Publ: Estudo de Avaliação
Responsável: CL1.1 - Biblioteca Central


  5 / 299 LILACS  
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Id: biblio-950900
Autor: Niu, Xiao-Ling; Hou, Jian-Feng; Li, Jing-Xiang.
Título: The NK1 receptor antagonist NKP608 inhibits proliferation of human colorectal cancer cells via Wnt signaling pathway
Fonte: Biol. Res;51:14, 2018. graf.
Idioma: en.
Projeto: Shanghai Pudong New Area Zhoupu Hospital College; . Shanghai Pudong New Area Health System.
Resumo: BACKGROUND: Neurokinin1 (NK1) receptor has played a vital role in the development of tumor. However, NKP608 as a NK1 receptor antagonist whether has the effect of the resistance of colorectal cancer is still unclear. Thereby, in this study, we investigated the role of NKP608 on human colorectal cancer and explored the underlying mechanism. METHODS: The cell proliferation of colorectal cancer cells was detected by cell counting kit-8 (CCK8) assay, cell migration and invasion were assessed by transwell assay, the apoptotic ratio of cells was assessed by Annexin V-fluorescein isothiocyanate/propidium iodide stained and flow cytometry. The involvement of molecular mechanisms was examined by western blot. RESULTS: In this study, we found that NKP608 inhibited the proliferation, migration/invasion of HCT116 cells. In addition, NKP608 reduced expressions of Wnt-3a, ß-catenin, Cyclin D1, and (vascular endothelial growth factor) VEGF while induced expression of E-Cadherin. Furthermore, flow cytometry analyzed that NKP608 induced apoptosis of HCT116 cells, consistently, western blotting detecting of apoptosis-related proteins revealed that NKP608 downregulated Bcl-2 while upregulated Bax and Active-Caspase-3. CONCLUSIONS: Taken together, our results demonstrated that NKP608 inhibited colorectal cancer cell proliferation, migration and invasion via suppressing the Wnt/ß-catenin signaling pathway. Therefore, NKP608 might represent a promising therapeutic agent in the treatment of colorectal cancer.
Descritores: Piperidinas/farmacologia
Quinolinas/farmacologia
Neoplasias Colorretais/patologia
Movimento Celular/efeitos dos fármacos
Proliferação de Células/efeitos dos fármacos
Via de Sinalização Wnt/efeitos dos fármacos
Antagonistas do Receptor de Neuroquinina-1/farmacologia
-Regulação para Baixo/efeitos dos fármacos
Western Blotting
Linhagem Celular Tumoral
Células HCT116
Citometria de Fluxo
Limites: Humanos
Responsável: CL1.1 - Biblioteca Central


  6 / 299 LILACS  
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Id: biblio-950902
Autor: Liu, Ping; Yu, Junyan; Tian, Xiangyang; Chang, Jianlan; Zhang, Ying; Zhang, Rong; Zhang, Ningning; Huang, Ranxing; Li, Lulu; Qiao, Xianli; Guo, Hongliang.
Título: The effect of downregulation of Stathmin gene on biological behaviors of U373 and U87-MG glioblastoma cells
Fonte: Biol. Res;51:16, 2018. tab, graf.
Idioma: en.
Resumo: BACKGROUND: Stathmin as a critical protein involved in microtubule polymerization, is necessary for survival of cancer cells. However, extremely little is known about Stathmin in glioblastoma. So, this study was designed to elucidate the function of Stathmin gene in the tumorigenesis and progression of glioblastoma cells. METHOD: The lentiviral interference vector pLV3-si-Stathmin targeting Stathmin gene and the control vector pLV3-NC were established for the co-transfection of 293T cells together with the helper plasmids. Viral titer was determined via limiting dilution assay. Then pLV3-si-Stathmin and pLV3-NC were stably co-transfected into U373 and U87-MG glioblastoma cells. Expression levels of Stathmin protein in each group were determined by using Western Blot, and the proliferation and migration ability of the cells with downregulated Stathmin were evaluated through CCK8 assay and transwell invasion assay, respectively. Cell cycles and cell apoptosis were detected with flow cytometry. Finally, the effect of Stathmin in tumor formation was determined in nude mice. RESULT: DNA sequencing and viral titer assay indicated that the lentiviral interference vector was successfully established with a viral titer of 4 × 108 TU/ml. According to the results from Western Blotting, Stathmin protein expression level decreased significantly in the U373 and U87-MG cells after transfected with pLV3-si-Stathmin, respectively, compared with those transfected with pLV3-NC. In glioblastoma cells, the cell proliferation and migration were greatly inhibited after the downregulation of Stathmin protein. Flow cytometry showed that much more cells were arrested in G2/M phasein Stathmin downregulated group, compared with the non-transfection group and NC group. But Stathmin downregulation did not induce significant cell apoptosis. Tumor formation assay in nude mice showed that tumor formation was delayed after Stathmin downregulation, with a reduction in both tumor formation rate and tumor growth velocity. CONCLUSION: Stathmin downregulation affected the biological behaviors of U373 and U87-MG glioblastoma cells, inhibiting the proliferation and migration of tumor cells. Stathmin gene may serve as a potential target in gene therapy for glioblastoma.
Descritores: Regulação para Baixo/genética
Glioblastoma/metabolismo
Proliferação de Células/genética
Estatmina/genética
-Transfecção
Glioblastoma/genética
Glioblastoma/patologia
Linhagem Celular Tumoral
Estatmina/metabolismo
Vetores Genéticos
Limites: Animais
Camundongos
Responsável: CL1.1 - Biblioteca Central


  7 / 299 LILACS  
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Id: biblio-950904
Autor: Xiong, Xilin; Li, Yang; Liu, Ling; Qi, Kai; Chen, Yueqin; Fang, Jianpei; Zhang, Chi.
Título: Arsenic trioxide induces cell cycle arrest and affects Trk receptor expression in human neuroblastoma SK-N-SH cells
Fonte: Biol. Res;51:18, 2018. tab, graf.
Idioma: en.
Projeto: Guangdong Science and Technology Department.
Resumo: BACKGROUND: Arsenic trioxide (As2O3), a drug that has been used in China for approximately two thousand years, induces cell death in a variety of cancer cell types, including neuroblastoma (NB). The tyrosine kinase receptor (Trk) family comprises three members, namely TrkA, TrkB and TrkC. Various studies have confirmed that TrkA and TrkC expression is associated with a good prognosis in NB, while TrkB overexpression can lead to tumor cell growth and invasive metastasis. Previous studies have shown that As2O3 can inhibit the growth and proliferation of a human NB cell line and can also affect the N-Myc mRNA expression. It remains unclear whether As2O3 regulates Trks for the purposes of treating NB. METHODS: The aim of the present study was to investigate the effect of As2O3 on Trk expression in NB cell lines and its potential therapeutic efficacy. SK-N-SH cells were grown with increasing doses of As2O3 at different time points. We cultured SK-N-SH cells, which were treated with increasing doses of As2O3 at different time points. Trk expression in the NB samples was quantified by immunohistochemistry, and the cell cycle was analyzed by flow cytometry. TrkA, TrkB and TrkC mRNA expression was evaluated by real-time PCR analysis. RESULTS: Immunohistochemical and real-time PCR analyses indicated that TrkA and TrkC were over-expressed in NB, and specifically during stages 1, 2 and 4S of the disease progression. TrkB expression was increased in stage 3 and 4 NB. As2O3significantly arrested SK-N-SH cells in the G2/M phase. In addition, TrkA, TrkB and TrkC expression levels were significantly upregulated by higher concentrations of As2O3 treatment, notably in the 48-h treatment period. Our findings suggested that to achieve the maximum effect and appropriate regulation of Trk expression in NB stages 1, 2 and 4S, As2O3 treatment should be at relatively higher concentrations for longer delivery times;however, for NB stages 3 and 4, an appropriate concentration and infusion time for As2O3 must be carefully determined. CONCLUSION: The present findings suggested that As2O3 induced Trk expression in SK-N-SH cells to varying degrees and may be a promising adjuvant to current treatments for NB due to its apoptotic effects.
Descritores: Óxidos/farmacologia
Arsenicais/farmacologia
Glicoproteínas de Membrana/efeitos dos fármacos
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Receptor trkB/efeitos dos fármacos
Proliferação de Células/efeitos dos fármacos
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Neuroblastoma/metabolismo
-Glicoproteínas de Membrana/metabolismo
Receptor trkB/metabolismo
Linhagem Celular Tumoral/efeitos dos fármacos
Linhagem Celular Tumoral/metabolismo
Trióxido de Arsênio
Neuroblastoma/patologia
Limites: Humanos
Responsável: CL1.1 - Biblioteca Central


  8 / 299 LILACS  
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Id: biblio-950907
Autor: Meng, Minjun; Chen, Yanling; Jia, Jianbo; Li, Lianghui; Yang, Sumei.
Título: Knockdown of PAICS inhibits malignant proliferation of human breast cancer cell lines
Fonte: Biol. Res;51:24, 2018. tab, graf.
Idioma: en.
Resumo: BACKGROUND: Phosphoribosylaminoimidazole carboxylase, phosphoribosylaminoimidazole succinocarboxamide synthetase (PAICS), an enzyme required for de novo purine biosynthesis, is associated with and involved in tumorigenesis. This study aimed to evaluate the role of PAICS in human breast cancer, which remains the most frequently diagnosed cancer and the leading cause of cancer-related death among women in less developed countries. RESULTS: Lentivirus-based short hairpin RNA targeting PAICS specifically depleted its endogenous expression in ZR-75-30 and MDA-MB-231 breast cancer cells. Depletion of PAICS led to a significant decrease in cell viability and proliferation. To ascertain the mechanisms through which PAICS modulates cell proliferation, flow cytometry was performed, and it was confirmed that G1-S transition was blocked in ZR-75-30 cells through PAICS knockdown. This might have occurred partly through the suppression of Cyclin E and the upregulation of Cyclin D1, P21, and CDK4. Moreover, PAICS knockdown obviously promoted cell apoptosis in ZR-75-30 cells through the activation of PARP and caspase 3 and downregulation of Bcl-2 and Bcl-xl expression in ZR-75-30 cells. CONCLUSIONS: These findings demonstrate that PAICS plays an essential role in breast cancer proliferation in vitro, which provides a new opportunity for discovering and identifying novel effective treatment strategies.
Descritores: Peptídeo Sintases/fisiologia
Neoplasias da Mama/enzimologia
Neoplasias da Mama/patologia
Carboxiliases/biossíntese
Biomarcadores Tumorais/fisiologia
Proliferação de Células
-Peptídeo Sintases/genética
Regulação Enzimológica da Expressão Gênica
Regulação Neoplásica da Expressão Gênica
Linhagem Celular Tumoral
Técnicas de Silenciamento de Genes
Citometria de Fluxo
Limites: Humanos
Feminino
Responsável: CL1.1 - Biblioteca Central


  9 / 299 LILACS  
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Id: biblio-983940
Autor: Sagredo, Eduardo A; Blanco, Alejandro; Sagredo, Alfredo I; Pérez, Paola; Sepúlveda-Hermosilla, Gonzalo; Morales, Fernanda; Müller, Bettina; Verdugo, Ricardo; Marcelain, Katherine; Harismendy, Olivier; Armisén, Ricardo.
Título: ADAR1-mediated RNA-editing of 3'UTRs in breast cancer
Fonte: Biol. Res;51:36, 2018. graf.
Idioma: en.
Projeto: FONDECYT; . NCI-Leidos; . NIH; . Anillo en Ciencia y Tecnología; . FONDEF; . CORFO.
Resumo: BACKGROUND: Whole transcriptome RNA variant analyses have shown that adenosine deaminases acting on RNA ( ADAR ) enzymes modify a large proportion of cellular RNAs, contributing to transcriptome diversity and cancer evolution. Despite the advances in the understanding of ADAR function in breast cancer, ADAR RNA editing functional consequences are not fully addressed. RESULTS: We characterized A to G(I) mRNA editing in 81 breast cell lines, showing increased editing at 3'UTR and exonic regions in breast cancer cells compared to immortalized non-malignant cell lines. In addition, tumors from the BRCA TCGA cohort show a 24% increase in editing over normal breast samples when looking at 571 well-characterized UTRs targeted by ADAR1. Basal-like subtype breast cancer patients with high level of ADAR1 mRNA expression shows a worse clinical outcome and increased editing in their 3'UTRs. Interestingly, editing was particularly increased in the 3'UTRs of ATM, GINS4 and POLH transcripts in tumors, which correlated with their mRNA expression. We confirmed the role of ADAR1 in this regulation using a shRNA in a breast cancer cell line (ZR-75-1). CONCLUSIONS: Altogether, these results revealed a significant association between the mRNA editing in genes related to cancer-relevant pathways and clinical outcomes, suggesting an important role of ADAR1 expression and function in breast cancer.
Descritores: Neoplasias da Mama/genética
Adenosina Desaminase/genética
Proteínas de Ligação a RNA/genética
Edição de RNA/genética
Regiões não Traduzidas/genética
Estabilidade de RNA/genética
-Neoplasias da Mama/metabolismo
Regulação Neoplásica da Expressão Gênica
Adenosina Desaminase/metabolismo
Proteínas de Ligação a RNA/metabolismo
Perfilação da Expressão Gênica
Estabilidade de RNA/fisiologia
Linhagem Celular Tumoral
Limites: Humanos
Feminino
Responsável: CL1.1 - Biblioteca Central


  10 / 299 LILACS  
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Id: biblio-983941
Autor: Wu, Milu; Fan, Baohua; Guo, Qijing; Li, Yan; Chen, Rong; Lv, Nannan; Diao, Yinzhuo; Luo, Yushuang.
Título: Knockdown of SETDB1 inhibits breast cancer progression by miR-381-3p-related regulation
Fonte: Biol. Res;51:39, 2018. graf.
Idioma: en.
Projeto: National Natural Science Foundation of China; . Scientific Research Project Funds of Qinghai Department.
Resumo: BACKGROUND: SET domain bifurcated 1 (SETDB1) has been widely considered as an oncogene playing a critical role in many human cancers, including breast cancer. Nevertheless, the molecular mechanism by which SETDB1 regulates breast cancer tumorigenesis is still unknown. METHODS: qRT-PCR assay or western blot analysis was performed to assess the expression level of SETDB1 mRNA or protein, respectively. siSETDB1, pCMV6-XL5-SETDB1, miR-381-3p mimic, or miR-381-3p inhibitor was transfected into cells to regulate the expression of SETDB1 or miR-381-3p. MiRNA directly interacted with SETDB1 was verified by luciferase reporter assay and RNA immunoprecipitation. CCK-8 assay, colony formation assay, flow cytometric analysis, and transwell assay were used to detect the abilities of cell proliferation, cell cycle progression and migration, respectively. Animal model of xenograft tumor was used to observe the regulatory effect of SETDB1 on tumor growth in vivo. RESULTS: We verified that SETDB1 mRNA level was upregulated in breast cancer tissues and cell lines, and SETDB1 depletion led to a suppression of cell proliferation, cell cycle progression and migration in vitro, as well as tumor growth in vivo. SETDB1 was verified to be a target of miR-381-3p. Moreover, miR-381-3p overexpression suppressed cell proliferation, cell cycle progression and migration, whereas SETDB1 abated miR-381-3p-mediated regulatory function on breast cancer cells. CONCLUSIONS: This study revealed that SETDB1 knockdown might suppress breast cancer progression at least partly by miR-381-3p-related regulation, providing a novel prospect in breast cancer therapy.
Descritores: Metiltransferases de Proteína/genética
Neoplasias da Mama/genética
MicroRNAs/metabolismo
-Metiltransferases de Proteína/metabolismo
Células-Tronco
Neoplasias da Mama/patologia
Histona-Lisina N-Metiltransferase
Reação em Cadeia da Polimerase Via Transcriptase Reversa
MicroRNAs/genética
Linhagem Celular Tumoral
Proliferação de Células
Modelos Animais de Doenças
Técnicas de Silenciamento de Genes
Citometria de Fluxo
Camundongos Endogâmicos BALB C
Limites: Humanos
Animais
Masculino
Feminino
Camundongos
Responsável: CL1.1 - Biblioteca Central



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