scholarly journals Association between transforming growth factor-β1 expression and the clinical features of triple negative breast cancer

2016 ◽  
Vol 11 (6) ◽  
pp. 4040-4044 ◽  
Author(s):  
MING-JIAN DING ◽  
KE SU ◽  
GUO-ZHONG CUI ◽  
WEN-HUA YANG ◽  
LIANG CHEN ◽  
...  
Nanoscale ◽  
2021 ◽  
Author(s):  
Jitang Chen ◽  
Si Li ◽  
Xin Liu ◽  
Sha Liu ◽  
Chen Xiao ◽  
...  

Photodynamic therapy (PDT) is frequently used for cancer treatment in the clinical settings. However, its applications in stroma-rich solid tumors, e.g., triple negative breast cancer, are limited by the abnormal...


2021 ◽  
Author(s):  
Hong Kyu Lee ◽  
Hyeong-Jin Ji ◽  
Sang-Kyung Shin ◽  
Jihye Koo ◽  
Tae Hun Kim ◽  
...  

Abstract Background: Transforming growth factor (TGF-β) pathway mediates suppression of anti-tumor immunity, and is associated with poor prognosis in triple-negative breast cancer (TNBC). Methods: In this study, we generated a humanized animal model by transplanting human peripheral blood mononuclear cells into immunodeficient mice followed by inoculation of MDA-MB-231 cells, and subsequently analyzed the role of TGF-β2 in the interaction between human T cells and human tumor cells. Results: Following reconstitution of the human immune system, inhibition of TGF-β signaling by TGF-β2 antisense oligodeoxynucleotide (TASO) resulted in accelerated tumor growth inhibition. TGF-β2 inhibition also resulted in downregulation of peripheral Foxp3+ regulatory T cells (Treg), whereas no effect was seen in the expression of CD8+ cytotoxic T cells. Analysis of the TASO-treated mice serum revealed elevated levels of human IFN-γ and reduced levels of human IL-10 and TGF-β2. Moreover, TGF-β2 inhibition resulted in increased CD8+ T cell infiltration, whereas the reduced infiltration of Tregs into the tumor partly resulted from decreased expression of CCL22. Decreased intra-tumoral Tregs facilitated the activation of cytotoxic T cells, associated with increased granzyme B expression. Conclusion: These results indicate that TASO potentiated T-cell mediated antitumor immunity, and it is proposed that TGF-β2 may be a promising target in the immunotherapeutic strategy of TNBC.


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