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Nuclear Expression of p-STAT3 Is Associated with Poor Prognosis in ER(−) Breast Cancer

The activation of signal transducer and activator of transcription 3 (STAT3) has been reported in several types of cancer, where it acts as an oncogene. However, in breast cancer, the clinical role of STAT3 remains unclear. In the present study, the association between phosphorylated-STAT3 (p-STAT3)...

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Detalles Bibliográficos
Autores principales: Nakagawa, Tsuyoshi, Oda, Goshi, Kawachi, Hiroshi, Ishikawa, Toshiaki, Okamoto, Kentaro, Uetake, Hiroyuki
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8938801/
https://www.ncbi.nlm.nih.gov/pubmed/35314590
http://dx.doi.org/10.3390/clinpract12020020
Descripción
Sumario:The activation of signal transducer and activator of transcription 3 (STAT3) has been reported in several types of cancer, where it acts as an oncogene. However, in breast cancer, the clinical role of STAT3 remains unclear. In the present study, the association between phosphorylated-STAT3 (p-STAT3) expression and clinicopathological/biological factors was examined in each subtype. p-STAT3 expression was examined in 135 cases of breast cancer by immunohistochemistry. p-STAT3 expression was not associated with clinicopathological/biological factors and prognosis in a complete cohort of breast cancer cases. However, in patients with estrogen receptor-negative (ER(−)) breast cancer and triple-negative breast cancer (TNBC), multivariate analysis showed that higher p-STAT3 expression was significantly associated with a short relapse-free survival (p = 0.029, HR 5.37, 95%CI 1.19–24.29). TNBC patients with p-STAT3 overexpression were found to have a poor prognosis (p = 0.029, HR 5.37, 95%CI 1.19–24.29). On the other hand, in ER(+) breast cancer, p-STAT3 overexpression was associated with a favorable prognosis (p = 0.034, HR 9.48, 95%CI 1.18–76.21). The present results suggested that STAT3 expression may play a different role in ER(−) and ER(+) breast cancer. In the future, the pharmacological inhibition of STAT3 expression may serve as an effective therapeutic strategy for ER(−) breast cancer, particularly TNBC.