scholarly journals Micro-RNA 33b inhibits breast cancer migration and invasion through regulating epithelial-mesenchymal transition in HER2 positive breast cancer cell lines

2017 ◽  
Vol 28 ◽  
pp. vii19-vii20
Author(s):  
B. Pattanayak ◽  
A. Adam-Artigues ◽  
E. Tormo ◽  
I. Garrido ◽  
B. Pineda ◽  
...  
2021 ◽  
Author(s):  
Tao Xueqin ◽  
Mei Jinhong ◽  
Huang Yuping

Abstract Background: Emerging evidences have demonstrated that Ubiquitin-conjugating enzyme E2T (UBE2T) is dysregulated and play critical roles in various cancers. With the development of sequencing technology, studies have discovered that UBE2T is overexpressed in breast cancer tissues. However, the biological roles of UBE2T in breast cancer are still far to clear. In the present study, Methods: We analyzed the UBE2T expression in the Cancer Genome Atlas (TCGA) database. Quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to assess the expression of UBE2T in breast cancer cell lines. Cell proliferation, invasion and epithelial-mesenchymal transition (EMT) were determined by using CCK-8, EdU, Transwell and western blot assays.Results: UBE2T was highly expressed in breast cancer cell lines. Functional analysis revealed that silence or elevation of UBE2T inhibited or promoted the proliferation, migration, invasion and EMT and Wnt/β-catenin signaling pathway related markers of MCF-7 cells. Mechanically, blocking of Wnt/β-catenin pathway by XAV939 reversed the promotion effect of UBE2T overexpression on breast cancer cells’ proliferation, migration and invasion.Conclusion: Our findings emphasized that UBE2T may act as an oncogene via activating the Wnt/β-catenin pathway, which may provide a potential therapeutic target for the treatment of breast cancer.


2014 ◽  
Vol 148 (3) ◽  
pp. 697-697
Author(s):  
Brigid C. Browne ◽  
Alex J. Eustace ◽  
Susan Kennedy ◽  
Neil A. O’Brien ◽  
Kasper Pedersen ◽  
...  

Oncogene ◽  
2018 ◽  
Vol 38 (15) ◽  
pp. 2675-2689 ◽  
Author(s):  
Gabriela Paroni ◽  
Marco Bolis ◽  
Adriana Zanetti ◽  
Paolo Ubezio ◽  
Kristian Helin ◽  
...  

Life ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 868
Author(s):  
Babak Nami ◽  
Avrin Ghanaeian ◽  
Corbin Black ◽  
Zhixiang Wang

HER2 receptor tyrosine kinase (encoded by the ERBB2 gene) is overexpressed in approximately 25% of all breast cancer tumors (HER2-positive breast cancers). Resistance to HER2-targeting therapies is partially due to the loss of HER2 expression in tumor cells during treatment. However, little is known about the exact mechanism of HER2 downregulation in HER2-positive tumor cells. Here, by analyzing publicly available genomic data we investigate the hypothesis that epithelial-mesenchymal transition (EMT) abrogates HER2 expression by epigenetic silencing of the ERBB2 gene as a mechanism of acquired resistance to HER2-targeted therapies. As result, HER2 expression was found to be positively and negatively correlated with the expression of epithelial and mesenchymal phenotype marker genes, respectively. The ERBB2 chromatin of HER2-high epithelial-like breast cancer cells and HER2-low mesenchymal-like cells were found to be open/active and closed/inactive, respectively. Decreased HER2 expression was correlated with increased EMT phenotype, inactivated chromatin and lower response to lapatinib. We also found that induction of EMT in the HER2-positive breast cancer cell line BT474 resulted in downregulated HER2 expression and reduced trastuzumab binding. Our results suggest that ERBB2 gene silencing by epigenetic regulation during EMT may be a mechanism of de novo resistance of HER2-positive breast cancer cells to trastuzumab and lapatinib.


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