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El silenciamiento de CALB1 aumenta la radiosensibilidad del cáncer de próstata a través de la disfunción mitocondrial

Chen Gong¹, Senmao Li¹, Ye An²

¹Department of Urology, The Second Affiliated Hospital of Kunming Medical University, No. 347 Dianmian Street, Wuhua District, Kunming, 650101, Yunnan, China; Urological disease clinical medical center of Yunnan province, The Second Affiliated Hospital of Kunming Medical University, No. 347 Dianmian Street, Wuhua District, Kunming, 650101, Yunnan, China; Scientific and Technological Innovation Team of Basic and Clinical Research of Bladder Cancer in Yunnan Universities, The Second Affiliated Hospital of Kunming Medical University, No. 347 Dianmian Street, Wuhua District, Kunming, 650101, Yunnan, China.

|September 3, 2025

Resumen

La calbindina 1 (CALB1) impulsa el crecimiento del cáncer de próstata y la radioresistencia. El agotamiento de CALB1 induce la senescencia y aumenta la sensibilidad a la radiación, lo que lo convierte en un objetivo terapéutico potencial para el cáncer de próstata.

Área de la Ciencia:

En el campo de la oncología
Biología molecular
Señales de calcio

Sus antecedentes:

El cáncer de próstata es una causa importante de mortalidad por cáncer masculino.
La resistencia al tratamiento, en particular la radiorresistencia, limita la eficacia terapéutica.
La calbindina 1 (CALB1), una proteína que se une al calcio, está implicada en la progresión del cáncer.

Objetivo del estudio:

Para investigar el papel de CALB1 en la progresión del cáncer de próstata.
Determinar el impacto de CALB1 en la respuesta a la radiación en el cáncer de próstata.
Para aclarar el mecanismo de regulación que involucra a miR-186-5p y CALB1.

Principales métodos:

Análisis de la expresión de CALB1 en el cáncer de próstata utilizando conjuntos de datos públicos (GEO, TCGA).
Validación de la relación reguladora entre miR-186-5p y CALB1.
Estudios funcionales en células de cáncer de próstata, esferoides y xenografts que incluyen knockdown de CALB1, quelación de calcio e intervenciones mitocondriales.

Principales resultados:

CALB1 fue identificado como un objetivo de miR-186-5p regulado a la baja en el cáncer de próstata.
El silenciamiento de CALB1 inhibió el crecimiento tumoral al inducir la senescencia a través de la desregulación del calcio, la disfunción mitocondrial y el estrés oxidativo.
La depleción de CALB1 aumentó significativamente la radiosensibilidad in vitro e in vivo.

Conclusiones:

CALB1 juega un papel crucial en la regulación de la progresión del cáncer de próstata y la respuesta a la radiación mediante el mantenimiento de la homeostasis del calcio.
El agotamiento de CALB1 conduce a una sobrecarga de calcio y a una disfunción mitocondrial, aumentando así la radiosensibilidad.
CALB1 representa un objetivo terapéutico prometedor para superar la radiorresistencia en el cáncer de próstata.

Palabras clave:

CALB1 La homeostasis del calcio Envejecimiento celular Cáncer de próstata Radiosensibilidad miR-186-5p y sus derivados

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