Expression of Phosphatase and Tensin Homolog Deleted on Chromosome Ten on the Development of Cisplatin Resistance in Breast Cancer by TGF-β1 Signal Pathway

2021 ◽  
Vol 11 (10) ◽  
pp. 1900-1907
Author(s):  
Yuan-Ding Zhang ◽  
Zhen-Xia Wang ◽  
Yan Zhang ◽  
Jin Pei

Introduction: This study aims to evaluate the expression of PTEN on the development of cisplatin resistance in breast cancer by TGF-β1 signal pathway in order to investigate the prognostic value of PTEN and TGF-β1 for breast cancer. Material and Methods: In this study, HE staining, Immunohistochemical staining, Immunofluorescence and Western blotting were used to detect the expression of PTEN and TGF-β1 in breast cancer MCF-7 cells to explain clearly the relationship between PTEN and TGF-β1 on TGF-β1 treated MCF-7 Cells. Results: The experiment results showed the expression of PTEN and TGF-β1 in Human breast cancer increased obviously compared with paracancerous tissues (P < 0.05). The expression of PTEN and TGF-β1 was closely correlated with tumor size, distant metastasis, pathological stage and progesterone receptor status, but not with age and lymph node status. At the same time, the expression of PTEN and TGF-β1 in cisplatin-treated MCF-7 Cells reduced as compared with untreated breast cancer cells (P < 0.05). In addition, the expression of PTEN increased by TGF-β1 inducer treated Human Breast Cancer Cells. However, the expression of PTEN in TGF-β1 inhibitor treated Human Breast Cancer Cells was lower than in untreated breast cancer cells (P < 0.05). Conclusions: PTEN and TGF-β1 played an important role in Human Breast cancer. In addition, the expression of PTEN could be regulated by TGF-β1 in Cisplatin and TGF-β1 treated Human Breast Cancer Cells.

2003 ◽  
Vol 17 (10) ◽  
pp. 2002-2012 ◽  
Author(s):  
Olga A. Sukocheva ◽  
Lijun Wang ◽  
Nathaniel Albanese ◽  
Stuart M. Pitson ◽  
Mathew A. Vadas ◽  
...  

Abstract Current understanding of cytoplasmic signaling pathways that mediate estrogen action in human breast cancer is incomplete. Here we report that treatment with 17β-estradiol (E2) activates a novel signaling pathway via activation of sphingosine kinase (SphK) in MCF-7 breast cancer cells. We found that E2 has dual actions to stimulate SphK activity, i.e. a rapid and transient activation mediated by putative membrane G protein-coupled estrogen receptors (ER) and a delayed but prolonged activation relying on the transcriptional activity of ER. The E2-induced SphK activity consequently activates downstream signal cascades including intracellular Ca2+ mobilization and Erk1/2 activation. Enforced expression of human SphK type 1 gene in MCF-7 cells resulted in increases in SphK activity and cell growth. Moreover, the E2-dependent mitogenesis were highly promoted by SphK overexpression as determined by colony growth in soft agar and solid focus formation. In contrast, expression of SphKG82D, a dominant-negative mutant SphK, profoundly inhibited the E2-mediated Ca2+ mobilization, Erk1/2 activity and neoplastic cell growth. Thus, our data suggest that SphK activation is an important cytoplasmic signaling to transduce estrogen-dependent mitogenic and carcinogenic action in human breast cancer cells.


1993 ◽  
Vol 215 (3) ◽  
pp. 671-676 ◽  
Author(s):  
Noriyoshi KIDA ◽  
Tomoaki YOSHIMURA ◽  
Haruo TAKAHASHI ◽  
Seiji NAGAO ◽  
Yoshinori NOZAWA ◽  
...  

2020 ◽  
pp. 1-11
Author(s):  
Kaliana Larissa Machado ◽  
Poliana Camila Marinello ◽  
Thamara Nishida Xavier Silva ◽  
Cássio Fernando Nunes Silva ◽  
Rodrigo Cabral Luiz ◽  
...  

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