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1.
Zhongguo Yi Xue Ke Xue Yuan Xue Bao ; 38(3): 253-9, 2016 06 10.
Artigo em Inglês | MEDLINE | ID: mdl-27469907

RESUMO

Objective To study the effect of endometrial stem cells (EnSCs) derived cytokine cocktail (EdCC) on myocardial ischemic reperfusion injury (I/R) in a mouse model. Methods EdCC was concentrated from the culture medium of EnSCs with Millipore ultra-filtration technology and was administrated to a myocardial I/R mouse models through tail vein injection. The infarct area was determined by TTC/Evans Blue staining. The apoptotic cells were counted by TUNEL assay and the protein level of cleaved caspase 3 was evaluated by Western blotting. Results The EdCC extraction efficiency was (222.4±29.3) Μg/10(6) cells in every 24 h,but the protein gradually degraded under-80 ℃ storage. As compared with I/R group,100 Μg fresh EdCC decreased infarct area (P=0.001),reduced apoptotic nuclei in the infarct border (P=0.019),and inhibited cleaved caspase 3 expression (P=0.002). Increasing EdCC dosage did not further reduce the infarct area. The myocardial protective effect of EdCC diminished after 90 days' storage under-80 ℃. Conclusion EdCC reduces myocardial I/R injury through protecting cardiomyocytes from apoptosis within 30 days storage under-80 ℃.


Assuntos
Citocinas/uso terapêutico , Endométrio/citologia , Traumatismo por Reperfusão Miocárdica/terapia , Células-Tronco/citologia , Animais , Apoptose , Caspase 3/metabolismo , Células Cultivadas , Modelos Animais de Doenças , Feminino , Camundongos , Miócitos Cardíacos/efeitos dos fármacos
2.
Cancer Med ; 8(14): 6358-6369, 2019 10.
Artigo em Inglês | MEDLINE | ID: mdl-31466138

RESUMO

BACKGROUND: As an oncogene, long noncoding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) can promote tumor metastasis. Hyperexpression of MALAT1 has been observed in many malignant tumors, including hepatocellular carcinoma (HCC). However, the role and mechanism of MALAT1 in HCC remain unclear. METHODS: Thirty human HCC and paracancerous tissue specimens were collected, and the human hepatoma cell lines Huh7 and HepG2 were cultured according to standard methods. MALAT1 and Snail family zinc finger (Slug) expression were measured by real-time PCR, immunohistochemistry, and western blotting. Luciferase reporter assay and RNA immunoprecipitation (RIP) assay verified the direct interaction between miR-124-3p and Slug(SNAI2) or MALAT1. Wound healing and transwell assays were performed to examine invasion and migration, and a subcutaneous tumor model was established to measure tumor progression in vivo. RESULTS: MALAT1 expression was upregulated in HCC tissues and positively correlated with Slug expression. MALAT1 and miR-124-3p bind directly and reversibly to each other. MALAT1 silencing inhibited cell migration and invasion. miR-124-3p inhibited HCC metastasis by targeting Slug. CONCLUSIONS: MALAT1 regulates Slug through miR-124-3p, affecting HCC cell metastasis. Thus, the MALAT1/miR-124-3p/Slug axis plays an important role in HCC.


Assuntos
Carcinoma Hepatocelular/genética , Carcinoma Hepatocelular/patologia , Regulação Neoplásica da Expressão Gênica , Neoplasias Hepáticas/genética , Neoplasias Hepáticas/patologia , MicroRNAs/genética , RNA Longo não Codificante/genética , Fatores de Transcrição da Família Snail/genética , Adulto , Idoso , Animais , Linhagem Celular Tumoral , Modelos Animais de Doenças , Feminino , Técnicas de Silenciamento de Genes , Humanos , Imuno-Histoquímica , Masculino , Camundongos , Pessoa de Meia-Idade , Metástase Neoplásica , Estadiamento de Neoplasias , Prognóstico , Interferência de RNA , Curva ROC , Fatores de Transcrição da Família Snail/metabolismo , Ensaios Antitumorais Modelo de Xenoenxerto
3.
Oncotarget ; 7(40): 65553-65567, 2016 10 04.
Artigo em Inglês | MEDLINE | ID: mdl-27566588

RESUMO

EMT (epithelial-mesenchymal transition) occurs in a wide range of tumor types, and has been shown to be crucial for metastasis. Epigenetic modifications of histones contribute to chromatin structure and result in the alterations in gene expression. Tri-methylation of histone H3 lysine 4 (H3K4me3) is associated with the promoters of actively transcribed genes and can serve as a transcriptional on/off switch. RbBP5 is a component of the COMPASS/ -like complex, which catalyzes H3K4me3 formation. In this study, we found that in the process of TGF-Beta1 induced EMT in the prostate cancer cell line DU145, H3K4me3 enrichment and RbBP5 binding increased in the vicinity of Snail (SNAI1) transcription start site. Knocking-down of RbBP5 notably decreased Snail expression and EMT. Recruitment of RbBP5 and formation of H3K4me3 at Snail TSS during EMT depend on binding of SMAD2/3 and CBP at Snail TSS. This study links the SMAD2/3 signal with Snail transcription via a histone modification - H3K4me3. Furthermore, our research also demonstrates that RbBP5 and even WRAD may be a promising therapeutic candidates in treating prostate cancer metastasis, and that DU145 cells maintain their incomplete mesenchymal state in an auto/ paracrine manner.


Assuntos
Histonas/metabolismo , Complexos Multiproteicos/metabolismo , Proteínas Nucleares/metabolismo , Neoplasias da Próstata/metabolismo , Fatores de Transcrição da Família Snail/genética , Linhagem Celular Tumoral , Proteínas de Ligação a DNA , Epigênese Genética , Transição Epitelial-Mesenquimal/genética , Humanos , Masculino , Metilação , Proteínas Nucleares/genética , Fragmentos de Peptídeos/metabolismo , Neoplasias da Próstata/genética , Ligação Proteica , RNA Interferente Pequeno/genética , Sialoglicoproteínas/metabolismo , Proteína Smad2/metabolismo , Proteína Smad3/metabolismo , Sítio de Iniciação de Transcrição , Fator de Crescimento Transformador beta/metabolismo
4.
Chin J Cancer ; 35: 48, 2016 May 27.
Artigo em Inglês | MEDLINE | ID: mdl-27233483

RESUMO

The truncated chromosome 22 that results from the reciprocal translocation t(9;22)(q34;q11) is known as the Philadelphia chromosome (Ph) and is a hallmark of chronic myeloid leukemia (CML). In leukemia cells, Ph not only impairs the physiological signaling pathways but also disrupts genomic stability. This aberrant fusion gene encodes the breakpoint cluster region-proto-oncogene tyrosine-protein kinase (BCR-ABL1) oncogenic protein with persistently enhanced tyrosine kinase activity. The kinase activity is responsible for maintaining proliferation, inhibiting differentiation, and conferring resistance to cell death. During the progression of CML from the chronic phase to the accelerated phase and then to the blast phase, the expression patterns of different BCR-ABL1 transcripts vary. Each BCR-ABL1 transcript is present in a distinct leukemia phenotype, which predicts both response to therapy and clinical outcome. Besides CML, the Ph is found in acute lymphoblastic leukemia, acute myeloid leukemia, and mixed-phenotype acute leukemia. Here, we provide an overview of the clinical presentation and cellular biology of different phenotypes of Ph-positive leukemia and highlight key findings regarding leukemogenesis.


Assuntos
Proteínas de Fusão bcr-abl/genética , Leucemia Mielogênica Crônica BCR-ABL Positiva/genética , Leucemia Mieloide Aguda/genética , Leucemia-Linfoma Linfoblástico de Células Precursoras/genética , Carcinogênese , Proliferação de Células , Instabilidade Genômica , Humanos , Leucemia Mielogênica Crônica BCR-ABL Positiva/patologia , Leucemia Mieloide Aguda/patologia , Cromossomo Filadélfia , Leucemia-Linfoma Linfoblástico de Células Precursoras/patologia , Prognóstico , Proto-Oncogene Mas
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