The association between lncRNA H19 and EZH2 expression in patients with EBV-positive laryngeal carcinoma

Introducción: El cáncer es una enfermedad de alta incidencia, con múltiples factores etiológicos y diferentes características evolutivas. Objetivo: Describir la supervivencia y la tendencia de las tasas de incidencia y mortalidad por cáncer de laringe y senos paranasales en Cali (Colombia) durante el periodo 1962 a 2015. Diseño: Estudio observacional descriptivo. Métodos: La información de incidencia, durante el periodo 1962 a 2012, se obtuvo en el RPCC y la mortalidad entre 1984-2015 de la SSPM. Elcomportamiento de la tendencia se evaluó con el porcentaje de cambio anual (APC) y la supervivencia relativa se estimó con el método de Ederer II. La estadificación se realizó con la AJCC. Resultados: Durante 1962 a 2012, se diagnosticaron 1623 casos nuevos de cáncer, 85.2% (1383 casos) fueron de laringe y 14.8% (240 casos) sinunasal 76% fueron hombres y el CCE fue el tipo histológico más frecuente 84.1% y 59.6% en laringe y sinunasal respectivamente. Se observó una disminución significativa del riesgo de cáncer de laringe en ambos sexos, siendo mayor la disminución en hombres (APC=-1,1*(ICD95%: -1,6; -0,7)). La disminución en la tasa de incidencia de cáncer de laringe CEC fue mayor en hombres (APC=-1,1*(ICD95%: -1,6; -0,6)) durante 1962-2012. Las tasas de mortalidad disminuyeron significativamente (APC=-2,5 (ICD95%:-3,6 -1,5)). La supervivencia relativa a 5 años durante el periodo 2008-2012, 43,5%; 93 pacientes se estadificaron con supervivencia: T3-T4 (41,5%) y T1-T2 (55,0%). Conclusiones: El riesgo del cáncer de laringe y sinunasal escamocelular asociado al tabaquismo disminuyó de manera significativa en hombres y mujeres de Cali durante los últimos 53 años.

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Relationship of local recurrence with expression of protein P53 and PCNA in laryngeal carcinoma and its surgical margins

Academic Journal of Second Military Medical University ◽

10.3724/sp.j.1008.2008.00413 ◽

2009 ◽

Vol 28 (4) ◽

pp. 413-417

Author(s):

Guang-bin SUN ◽

Hai-hong TANG ◽

Qin FANG ◽

Shui-miao ZHOU ◽

Zhao-ji LI

Keyword(s):

Local Recurrence ◽

Laryngeal Carcinoma ◽

Surgical Margins ◽

Protein P53 ◽

Relationship Of

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Long Noncoding RNA SPRY4-IT1 Modulates Ketamine-Induced Neurotoxicity in Human Embryonic Stem Cell-Derived Neurons through EZH2

Developmental Neuroscience ◽

10.1159/000513535 ◽

2021 ◽

pp. 1-9

Author(s):

Jingyuan Huang ◽

Yan Xu ◽

Fang Wang ◽

Haili Wang ◽

Lu Li ◽

...

Keyword(s):

Long Noncoding Rna ◽

Noncoding Rna ◽

Embryonic Stem ◽

Protective Effects ◽

Tyrosine Kinase Signaling ◽

Ezh2 Expression ◽

Induced Neurons ◽

Neurite Degeneration ◽

Dose Dependent

Objective: This study aimed to investigate whether long noncoding RNA sprouty receptor tyrosine kinase signaling antagonist 4-intronic transcript 1 (SPRY4-IT1) is involved in the regulation of ketamine-induced neurotoxicity. Methods: Human embryonic stem cells (hESCs) were induced into neurons in vitro and treated with ketamine. Apoptosis and neurite degeneration assays were used to determine ketamine-induced neurotoxicity and qRT-PCR to determine SPRY4-IT1 expression. SPRY4-IT1 was downregulated in hESC-induced neurons to examine its regulation on ketamine-induced neurotoxicity. The correlation between enhancer of zeste homolog 2 (EZH2) and SPRY4-IT1 was also examined. EZH2 was upregulated in SPRY4-IT1-downregualted hESC-induced neurons to further examine its participation in SPRY4-IT1-mediated ketamine neurotoxicity. Results: Ketamine-induced dose-dependent apoptosis, neurite degeneration, and SPRY4-IT1 upregulation in hESC-induced neurons. Lentivirus-mediated SPRY4-IT1 downregulation protected ketamine neurotoxicity. EZH2 expression was positively correlated with SPRY4-IT1 in hESC-induced neurons. EZH2 overexpression markedly reversed the protective effects of SPRY4-IT1 knockdown on ketamine neurotoxicity. Conclusions: SPRY4-IT1 is involved in anesthesia-induced neurotoxicity, possibly through the regulation on EZH2 gene.

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A Plea for the “Window” Resection Method in Dealing with Certain Types of Laryngeal Carcinoma, with a Clinical History of Seven Cases

The Journal of Laryngology & Otology ◽

10.1017/s0022215100036975 ◽

1932 ◽

Vol 47 (2) ◽

pp. 81-91 ◽

Cited By ~ 1

Author(s):

Norman Patterson

Keyword(s):

Laryngeal Carcinoma ◽

Clinical History ◽

History Of ◽

Window Resection

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EZH2 reduction is an essential mechanoresponse for the maintenance of super-enhancer polarization against compressive stress in human periodontal ligament stem cells

Cell Death and Disease ◽

10.1038/s41419-020-02963-3 ◽

2020 ◽

Vol 11 (9) ◽

Author(s):

Qian Li ◽

Xiwen Sun ◽

Yunyi Tang ◽

Yanan Qu ◽

Yanheng Zhou ◽

...

Keyword(s):

Stem Cells ◽

Mechanical Stress ◽

Periodontal Ligament ◽

Compressive Force ◽

Mechanical Stimuli ◽

Periodontal Ligament Stem Cells ◽

Super Enhancer ◽

Ezh2 Expression ◽

A Genome ◽

Temporal Dimensions

Abstract Despite the ubiquitous mechanical cues at both spatial and temporal dimensions, cell identities and functions are largely immune to the everchanging mechanical stimuli. To understand the molecular basis of this epigenetic stability, we interrogated compressive force-elicited transcriptomic changes in mesenchymal stem cells purified from human periodontal ligament (PDLSCs), and identified H3K27me3 and E2F signatures populated within upregulated and weakly downregulated genes, respectively. Consistently, expressions of several E2F family transcription factors and EZH2, as core methyltransferase for H3K27me3, decreased in response to mechanical stress, which were attributed to force-induced redistribution of RB from nucleoplasm to lamina. Importantly, although epigenomic analysis on H3K27me3 landscape only demonstrated correlating changes at one group of mechanoresponsive genes, we observed a genome-wide destabilization of super-enhancers along with aberrant EZH2 retention. These super-enhancers were tightly bounded by H3K27me3 domain on one side and exhibited attenuating H3K27ac deposition and flattening H3K27ac peaks along with compensated EZH2 expression after force exposure, analogous to increased H3K27ac entropy or decreased H3K27ac polarization. Interference of force-induced EZH2 reduction could drive actin filaments dependent spatial overlap between EZH2 and super-enhancers and functionally compromise the multipotency of PDLSC following mechanical stress. These findings together unveil a specific contribution of EZH2 reduction for the maintenance of super-enhancer stability and cell identity in mechanoresponse.

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