Can estrogen receptor overexpression in normal tissues due to previous estrogen deprivation explain the fulvestrant efficacy in breast cancer therapy?

2012 ◽  
Vol 79 (6) ◽  
pp. 869-871 ◽  
Author(s):  
Sven Kurbel
2019 ◽  
Vol 20 (8) ◽  
pp. 665-673 ◽  
Author(s):  
Mohsen Mohammady ◽  
Seyed I. Ghetmiri ◽  
Mahtab Baharizade ◽  
Mohammad H. Morowvat ◽  
Susan Torabi

Background:One of the most prevalent cancers befell to women is considered to be breast cancer (BC). It is also the deadliest among the female population after lung cancer. Additionally, several studies have demonstrated that there is an association between microRNA34-a and breast cancer.Method:We searched PubMed, Web of Science, and Google Scholar up to December 2018. Those studies which have been studied miR-34a and its tumor-suppressing capabilities were considered as the most important topics. Moreover, we extracted articles which were solely focused on microRNA-34a in breast cancer therapy. Finally, 80 articles were included.Results:In comparison with the normal tissues, down-regulation of miR-34a expression is shown considerably in tumor cells. Overexpression of miR-34a acts as a tumor suppressor by transcriptional regulating one of the signaling pathways (TP53), NOTCH, and transforming growth factor beta (TGF-β), Bcl- 2 and SIRT1genes, HDAC1 and HDAC7, Fra-1, TPD52, TLR Via CXCL10. Moreover, drug resistance declines which lead to the apoptosis, cell cycle arrest and senescence. As a result, the proliferation, invasion and metastasis of the tumor are suppressed. The Mrx34 drug contains miR-34a mimic and a lipid vector. MiR-34a as the active ingredient portrays the role of a tumor suppressor. This drug has recently entered the clinical trials studies.Conclusion:These findings suggest a robust cause for developing miR-34a as a therapeutic agent to target BC. In that scenario, miR-34a is strongly useful to introduce new therapeutic goals for BC. Moreover, this review aims to confirm the signal pathways, therapeutic and diagnostic values of miR- 34a in BC and beyond.


2014 ◽  
pp. 1
Author(s):  
Jitender Madan ◽  
Sushma R. Gundala ◽  
Yoganjaneyulu Kasetti ◽  
Prasad V. Bharatam ◽  
Ritu Aneja ◽  
...  

2017 ◽  
Vol 8 (3) ◽  
pp. 135-142 ◽  
Author(s):  
Irida Kastrati ◽  
Marton I. Siklos ◽  
Svitlana D. Brovkovych ◽  
Gregory R. J. Thatcher ◽  
Jonna Frasor

2019 ◽  
Vol 14 (1) ◽  
pp. 688-698
Author(s):  
Zheng Ye ◽  
Zhaoyu Zhang ◽  
Lijiao Fang ◽  
Daiquan Tian ◽  
Xin Liu

AbstractObjectiveTo explore the potential role of GSG2 in breast cancer progression.MethodsThe mRNA expression, DNA copy number and clinical data used in this study were obtained from the TCGA data portal. The copy number variations (CNVs) thresholds were determined according to the set of discrete copy number calls provided by Genomic Identification of Significant Targets in Cancer (GISTIC).ResultsThe mRNA expression level of GSG2 in 112 breast cancer tissues was much higher than that in adjacent normal tissues. GSG2 was significantly upregulated in stage II compared with stage I, and there was no differential expression of GSG2 between tumors with or without metastasis. Heterozygous deletion occupied 57.1% of CNVs for GSG2 gene in breast cancer samples. Patients with higher GSG2 expression tended to suffer from poorer prognosis.ConclusionOur profiling analysis indicated the overexpression of GSG2 might play an important role in breast cancer development, suggesting that GSG2 could be a new target for breast cancer treatment, making GSG2 inhibitors becoming potential drugs for breast cancer therapy.


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