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Updated: Sep 9, 2025
07:02
In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
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La transcriptómica espacial revela la reprogramación transcriptómica y del microambiente inmune durante la
Kang Ning1,2,3, Bu Zou1,2,3, Yongchao Yu1,2,3
1Department of Head and Neck Surgery, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China.
Advanced science (Weinheim, Baden-Wurttemberg, Germany)
|September 5, 2025
Resumen
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.
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.
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