Upregulation of FGF9 and NOVA1 in cancer-associated fibroblasts promotes cell proliferation, invasion and migration of triple negative breast cancer.

Zhang, Bo; Liu, Yang; Yu, Jinsong; Lin, Xi

Zhang, Bo; Liu, Yang; Yu, Jinsong; Lin, Xi.

Afiliación

Zhang B; Department of Thyroid and Breast Surgery, Nanyang First People's Hospital, Nanyang, China.
Liu Y; Endocrinology Department of integrated Chinese and Western medicine, Nanyang Central Hospital, Nanyang, China.
Yu J; Department of Thyroid and Breast Surgery, Nanyang First People's Hospital affiliated to Henan University, Nanyang, China.
Lin X; Key Laboratory of Thyroid Tumor Prevention and Treatment, Nanyang First People's Hospital affiliated to Henan University, Nanyang, China.

Drug Dev Res ; 85(3): e22185, 2024 May.

Article en En | MEDLINE | ID: mdl-38657094

ABSTRACT

ABSTRACT

Cancer-associated fibroblasts (CAFs) play a pivotal role in cancer progression. This study aimed to explore the roles of CAFs-derived Fibroblast growth factor 9 (FGF9) and Neuro-oncological ventral antigen 1 (NOVA1) in triple negative breast cancer (TNBC) progression. MDA-MB-231 and BT-549 cells were cocultured with CAF conditioned-medium (CAF-CM) or normal fibroblasts conditioned-medium (NF-CM). MTT, EdU, colony formation, wound healing, transwell migration, and invasion assays were employed to determine cell proliferation, migration and invasion, respectively. Western blot and RT-qPCR were carried out to examine the protein and mRNA expression of FGF9 and NOVA1. Xenograft tumor experiments were conducted to evaluate the effects of CAFs, FGF9, and NOVA1 on tumor growth in vivo. Our results showed that CAFs significantly promoted the proliferation, invasion, and migration of TNBC cells. FGF9 and NOVA1 were significantly upregulated in TNBC CAFs, tissues and cells. CAF-CM also could increase the expression of FGF9 and NOVA1 in TNBC cells. Knockdown of FGF9 or NOVA1 could hamper cell proliferation, invasion, migration, and EMT of TNBC cells. Moreover, CAFs with FGF9/NOVA1 knockdown also could inhibit TNBC progression. Besides, CAFs significantly accelerated tumor growth in vivo, which was blocked by FGF9/NOVA1 knockdown in nude mice. In conclusion, our results indicated the tumor-promoting role of CAFs in TNBC progression. FGF9 and NOVA1 upregulation in CAFs induced cell proliferation, migration and invasion in vitro, and facilitated tumor growth in vivo in TNBC development.

Asunto(s)

Fibroblastos Asociados al Cáncer; Movimiento Celular; Proliferación Celular; Factor 9 de Crecimiento de Fibroblastos; Antígeno Ventral Neuro-Oncológico; Proteínas de Unión al ARN; Neoplasias de la Mama Triple Negativas; Animales; Femenino; Humanos; Ratones; Fibroblastos Asociados al Cáncer/metabolismo; Línea Celular Tumoral; Factor 9 de Crecimiento de Fibroblastos/genética; Factor 9 de Crecimiento de Fibroblastos/metabolismo; Regulación Neoplásica de la Expresión Génica; Ratones Endogámicos BALB C; Ratones Desnudos; Invasividad Neoplásica; Proteínas de Unión al ARN/genética; Proteínas de Unión al ARN/metabolismo; Neoplasias de la Mama Triple Negativas/genética; Neoplasias de la Mama Triple Negativas/patología; Neoplasias de la Mama Triple Negativas/metabolismo; Regulación hacia Arriba; Ensayos Antitumor por Modelo de Xenoinjerto

Palabras clave

FGF9; NOVA1; cancerassociated fibroblasts; triple negative breast cancer

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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Movimiento Celular / Proteínas de Unión al ARN / Proliferación Celular / Factor 9 de Crecimiento de Fibroblastos / Neoplasias de la Mama Triple Negativas / Fibroblastos Asociados al Cáncer / Antígeno Ventral Neuro-Oncológico Límite: Animals / Female / Humans Idioma: En Revista: Drug Dev Res Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Estados Unidos

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