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1.
Clin Transl Oncol ; 20(4): 534-541, 2018 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-28921460

RESUMEN

PURPOSE: The objective of the study was to investigate the role of NFBD1 in the proliferation and apoptosis of laryngeal squamous cell carcinoma (LSCC) cells. METHODS: Immunohistochemistry (IHC) and qRT-PCR was employed to determine the expressions of NFBD1 protein and mRNA in LSCC tissues and adjacent noncancerous tissues. After the downregulation of NFBD1 expression, the colony formation assay, MTS assay and apoptosis assay were used to investigate the changes in the proliferation and apoptosis of Hep2 cells. The mechanisms by which silencing NFBD1 promote apoptosis of Hep2 cells were examined by western blotting. Furthermore, xenograft models were used to evaluate the proliferation of Hep2 cells in vivo. RESULTS: NFBD1 protein was upregulated in 55.6% of LSCC cancer tissues compared with adjacent normal tissues (26.7%). NFBD1 knockdown in Hep2 cells significantly impacted proliferation and apoptosis, and silencing NFBD1 might promote apoptosis of Hep2 cells by activating the mitochondrial apoptotic pathway. Xenograft models showed that silencing NFBD1 also significantly inhibited tumor growth. CONCLUSIONS: Our data highlight that NFBD1 participates in the regulation of proliferation and apoptosis in LSCC, and suggest that NFBD1 could be a promising therapy target.


Asunto(s)
Carcinoma de Células Escamosas/patología , Neoplasias de Cabeza y Cuello/patología , Neoplasias Laríngeas/patología , Proteínas Nucleares/metabolismo , Transactivadores/metabolismo , Proteínas Adaptadoras Transductoras de Señales , Adulto , Anciano , Animales , Apoptosis/fisiología , Proteínas de Ciclo Celular , Proliferación Celular/fisiología , Femenino , Xenoinjertos , Humanos , Masculino , Ratones , Ratones Endogámicos BALB C , Ratones Desnudos , Persona de Mediana Edad , Carcinoma de Células Escamosas de Cabeza y Cuello
2.
Genet Mol Res ; 14(2): 4282-90, 2015 Apr 28.
Artículo en Inglés | MEDLINE | ID: mdl-25966200

RESUMEN

This study aimed to explore new opportunities for developing targeted therapy for triple-negative breast cancer (TNBC) by analyzing the significance and association between p53 and epidermal growth factor receptor (EGFR) expression in different molecular subtypes of breast cancer. The clinical and pathological data of 264 patients with breast cancer receiving surgery in our hospital from January 2012 to August 2013 were retrospectively analyzed. According to the expression of estrogen receptor, progesterone receptor, human epidermal growth factor receptor 2 (HER2), Ki-67, CK5/6, p53, and EGFR detected by immunohistochemical methods, breast cancer was divided into four molecular subtypes. Then, the expression of p53 and EGFR as well as their correlation in the different subtypes were determined. Among the four subtypes, luminal B breast cancer was the most common type. TNBC and HER2-enriched breast cancer had larger tumor sizes with higher expression of Ki-67 as compared with the luminal types. TNBC had a lower lymph node metastasis rate but higher CK5/6 and EGFR expression than the other three types. The expression of p53 was higher in luminal B, HER2-enriched, and triple-negative breast cancers, and this was positively correlated with the expression of EGFR in TNBC but not in the other subtypes. p53 and EGFR expression was positively correlated in TNBC, which enables us to explore the molecular biological characteristics of TNBC, so as to provide new ideas for the treatment of TNBC.


Asunto(s)
Biomarcadores de Tumor/metabolismo , Receptores ErbB/metabolismo , Neoplasias de la Mama Triple Negativas/clasificación , Neoplasias de la Mama Triple Negativas/patología , Proteína p53 Supresora de Tumor/metabolismo , Adulto , Anciano , Femenino , Humanos , Antígeno Ki-67/biosíntesis , Persona de Mediana Edad , Terapia Molecular Dirigida/métodos , Receptor ErbB-2/metabolismo , Receptores de Estrógenos/metabolismo , Receptores de Progesterona/metabolismo , Estudios Retrospectivos , Neoplasias de la Mama Triple Negativas/genética
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