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TNFAIP3 mediates FGFR1 activation-induced breast cancer angiogenesis by promoting VEGFA expression and secretion
Gao, Mengdi; Li, Xue; Yang, Mao; Feng, WanRu; Lin, Yan; He, Tao.
Afiliación
  • Gao, Mengdi; Southwest Medical University. Institute for Cancer Medicine and School of Basic Medical Sciences. Luzhou. China
  • Li, Xue; Southwest Medical University. Institute for Cancer Medicine and School of Basic Medical Sciences. Luzhou. China
  • Yang, Mao; Southwest Medical University. Institute for Cancer Medicine and School of Basic Medical Sciences. Luzhou. China
  • Feng, WanRu; Southwest Medical University. Institute for Cancer Medicine and School of Basic Medical Sciences. Luzhou. China
  • Lin, Yan; Southwest Medical University. Institute for Cancer Medicine and School of Basic Medical Sciences. Luzhou. China
  • He, Tao; Southwest Medical University. Institute for Cancer Medicine and School of Basic Medical Sciences. Luzhou. China
Clin. transl. oncol. (Print) ; 24(12): 2453-2465, dec. 2022.
Article en En | IBECS | ID: ibc-216091
Biblioteca responsable: ES1.1
Ubicación: ES15.1 - BNCS
ABSTRACT
Purpose To investigate the role and mechanism of TNF-inducible protein 3(TNFAIP3) in breast cancer angiogenesis induced by fibroblast growth factor receptor1 (FGFR1) activation. Methods The immunohistochemical assay was used to detect the expression of vascular endothelial cell marker CD31 and CD105 in mice DCIS.COM-iFGFR1 transplanted tumor (previously established by our group). The effects of TNFAIP3 knockout/knockdown breast cancer cell lines on angiogenesis, migration, and invasion of Human Umbilical Vein Endothelial Cells (HUVEC) were detected by the tubulogenesis and Trewells assay. RNA-seq analysis of TNFAIP3 downstreams differential genes after TNFAIP3 knockdown. The expression and secretion of VEGFA after FGFR1 activation in breast cancer cells were detected by qPCR, Western blot, and ELISA. Results Immunohistochemistry showed that TNFAIP3 knockout inhibited the expression of CD31 and CD105 in DCIS grafted tumors promoted by FGFR1 activation. Tubulogenesis and Trewells experiments showed that TNFAIP3 gene knockout/knockdown inhibited the angiogenesis, migration, and invasion of HUVEC cells promoted by FGFR1 activation. qPCR assay showed that VEGFA mRNA level in the TNFAIP3 knockdown cell line was significantly down-regulated (p < 0.05). qPCR, Western blot and ELISA results showed that TNFAIP3 gene knockout/knockdown could inhibit the expression and secretion of VEGFA in breast cancer cells induced by FGFR1 activation. Conclusion TNFAIP3 promotes breast cancer angiogenesis induced by FGFR1 activation through the expression and secretion of VEGFA. (AU)
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Colección: 06-national / ES Base de datos: IBECS Asunto principal: Neoplasias de la Mama / Carcinoma Intraductal no Infiltrante Límite: Animals / Female / Humans Idioma: En Revista: Clin. transl. oncol. (Print) Año: 2022 Tipo del documento: Article
Buscar en Google
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Colección: 06-national / ES Base de datos: IBECS Asunto principal: Neoplasias de la Mama / Carcinoma Intraductal no Infiltrante Límite: Animals / Female / Humans Idioma: En Revista: Clin. transl. oncol. (Print) Año: 2022 Tipo del documento: Article