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Physapubescin induced human breast cancer MCF-7 cells apoptosis by inhibiting STAT3
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DOI   10.11656/j.issn.1673-9043.2024.01.02
Key Words   human breast cancer MCF-7 cell;Physapubescin;apoptosis;TAT3
Author NameAffiliationE-mail
HAN Hongye School of Intergrative Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China
School of Medical Technology, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China 
 
YU Yaqin School of Intergrative Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China
Department of Oncology, Wuhan Huangpi District People's Hospital, Wuhan 430300, China 
 
ZHANG Qiang School of Medical Technology, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China  
SUN Yujie School of Medical Technology, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China  
KANG Ning School of Medical Technology, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China kangndd@163.com 
Abstract
    [Objective] This study determined the role of signal transducer and activator of transcription 3(STAT3) in Physapubescin(PPB) induced apoptosis in the human breast cancer MCF-7 cells. [Methods] The fluorescent stain technology was used to analyze that PPB induced MCF-7 cells apoptosis. The potential mechanisms of PPB against breast cancer were predicted by bioinformatics analysis. The MTT assay was used to investigate the effects of STAT3 inhibitor S3I-201 and STAT3 small interfering RNA(siRNA) on the inhibition of MCF-7 cell growth by PPB. The effects of PPB alone or pretreatment with STAT3 siRNA on the expression of STAT3, B-cell lymphoma-2(Bcl-2), Bcl-2 Associated X protein(Bax), Caspase8, Caspase9, Cytochrome c and poly polymerase(PARP) proteins in MCF-7 cells were detected by Western Blot. [Results] The apoptotic morphology of MCF-7 cells was distinctly characterized by the effect of PPB, and the apoptosis ratio was significantly increased.The bioinformatics analysis showed that STAT3, a common target of PPB and breast cancer disease, was highly expressed in breast cancer tissues, and single-gene GSEA results suggested that high STAT3 expression was negatively correlated with the apoptotic signaling pathway. The results of Western Blot showed that PPB could inhibit STAT3 phosphorylation. The S3I-201 inhibitor or STAT3 siRNA could further promote PPB to inhibit MCF-7 cell growth. In addition, knockdown of STAT3 further increased the up-regulation of PPB on the pro-apoptotic proteins Bax, Cytochrome c, Cleaved-Caspase8, Cleaved-Caspase9, and Cleaved-PARP, meanwhile the inhibitory effect of PPB on the expression of anti-apoptotic protein Bcl-2 was enhanced by treatment with STAT3 siRNA. [Conclusion] PPB induced human breast cancer MCF-7 cells apoptosis by inhibiting STAT3.

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