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Low blood levels of the thyroid hormones — triiodothyronine (T3) and thyroxine (T4) — signal the hypothalamus to release the thyrotropin-releasing hormone (TRH). TRH then reaches the pituitary gland and stimulates the release of thyroid-stimulating hormone(TSH) into the bloodstream.
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In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

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La transcriptómica espacial revela la reprogramación transcriptómica y del microambiente inmune durante la

Kang Ning^1,2,3, Bu Zou^1,2,3, Yongchao Yu^1,2,3

¹Department of Head and Neck Surgery, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China.

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Resumen

Este resumen es generado por máquina.

El carcinoma de tiroides anaplásico (ATC) evoluciona desde el carcinoma de tiroides diferenciado (DTC) a través de cambios genómicos y supresión inmune. La pérdida de PDCD4 impulsa la infiltración de macrófagos asociados al tumor, crucial para la progresión de la ATC.

Palabras clave:

Los macrófagos M2 En el caso de las personas físicas Carcinoma de tiroides anaplásico Cáncer de tiroides diferenciado Transcriptómica espacial y sus aplicaciones

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Área de la Ciencia:

En el campo de la oncología
La genómica
Inmunología

Sus antecedentes:

El carcinoma de tiroides anaplásico (ATC) es un cáncer altamente letal.
El ATC a menudo surge de un carcinoma de tiroides diferenciado (DTC) a través de un proceso de desdiferenciación mal entendido.

Objetivo del estudio:

Para aclarar los mecanismos moleculares que impulsan la transición de DTC a ATC.
Identificar los reguladores clave y los actores celulares en la desdiferenciación del cáncer de tiroides.

Principales métodos:

Secuenciación transcriptómica espacial (spRNAseq) en regiones DTC y ATC coexistentes.
Secuenciación de todo el exoma e inferencia del análisis CNV.
Análisis de trayectoria y experimentos mecanicistas.

Principales resultados:

ATC exhibe supresión inmune regulada, angiogénesis y genes de remodelación de ECM.
Las regiones DTC adyacentes muestran alteraciones genómicas tempranas que preparan para la desdiferenciación.
PDCD4 y TYMP son reguladores clave de la desdiferenciación del cáncer de tiroides.
Los macrófagos asociados al tumor TYMP+ (TAM) están enriquecidos en ATC, promoviendo la inmunosupresión.
La pérdida de PDCD4 promueve la infiltración de TAM a través de vías dependientes de eIF4A.

Conclusiones:

El DTC con alteraciones genómicas similares al ATC se somete a una reprogramación transcriptómica e inmune para convertirse en ATC.
La formación de TAM inducida por la pérdida de PDCD4 es crítica para el desarrollo y la progresión de ATC.