scholarly journals Erythrocyte membrane protein band 4.1-like 3 inhibits osteosarcoma cell invasion through regulation of Snai1-induced epithelial-to-mesenchymal transition

Aging ◽  
2020 ◽  
Author(s):  
Xiaofeng Yuan ◽  
Lianhua Piao ◽  
Luhui Wang ◽  
Xu Han ◽  
Lei Tong ◽  
...  
2018 ◽  
Vol 51 (2) ◽  
pp. 938-948 ◽  
Author(s):  
Yazeng Huang ◽  
Jun Zhang ◽  
Haiyu Shao ◽  
Jianwen Liu ◽  
Mengran Jin ◽  
...  

Background/Aims: Preventing cell metastasis is an effective therapeutic strategy to treat osteosarcoma and improve prognosis. Statins have been found to have anticancer effects in addition to their cholesterol-lowering action. As a new target of statins, cysteine-rich 61 (CYR61) was recently identified to promote cell migration and metastasis in osteosarcoma. However, the underlying mechanisms mediating the regulation of CYR61 expression by statins remain unknown. Methods: Human osteosarcoma cell lines MG63 and SaOS2 were used to clarify the effect of lovastatin on CYR61 expression. Real-time PCR was performed to detect mRNA or microRNA (miRNA) levels and western blot was performed to detect protein levels. Cell invasive ability was determined using Transwell assays. Lentivirus encoding CYR61 cDNA or sterol regulatory element-binding protein 2 (SREBP-2) shRNA was used to upregulate CYR61 expression or downregulate SREBP-2 expression. Binding of the CYR61 3’ untranslated region (UTR) and miR-33a was analyzed by luciferase reporter assay. Results: We found that lovastatin treatment decreased CYR61 expression, inhibited cell invasion and altered epithelial-to-mesenchymal-transition (EMT)-related protein expression, while CYR61 overexpression abolished the effect of lovastatin. Moreover, lovastatin increased the expression of SREBP-2 and miR-33a, which were then downregulated by SREBP-2 silencing. Bioinformatics analysis indicated that the CYR61 3′UTR harbored a potential miR-33a binding site and luciferase reporter assay demonstrated that CYR61 was a target of miR-33a in osteosarcoma cells. Furthermore, miR-33a could inhibit cell invasion and alter EMT-related protein expression. SREBP-2 silencing or miR-33a inhibitor upregulated CYR61 expression and reversed the effects of lovastatin on cell invasion and EMT-related proteins. Conclusion: Our findings suggest lovastatin suppresses osteosarcoma cell invasion through the SREBP-2/miR-33a/CYR61 pathway.


1989 ◽  
Vol 264 (27) ◽  
pp. 15893-15899 ◽  
Author(s):  
B M Willardson ◽  
B J M Thevenin ◽  
M L Harrison ◽  
W M Kuster ◽  
M D Benson ◽  
...  

2021 ◽  
Author(s):  
Shahan Mamoor

Breast cancer affects women at relatively high frequency (1). We mined published microarray datasets (2, 3) to determine in an unbiased fashion and at the systems level genes most differentially expressed in the primary tumors of patients with breast cancer. We report here significant differential expression of the gene encoding erythrocyte membrane protein band 4.2, EPB42, when comparing primary tumors of the breast to the tissue of origin, the normal breast. EPB42 mRNA was present at significantly lower quantities in tumors of the breast as compared to normal breast tissue. Analysis of human survival data revealed that expression of EPB42 in primary tumors of the breast was correlated with overall survival in patients with normal-like subtype cancer, demonstrating a relationship between primary tumor expression of a differentially expressed gene and patient survival outcomes influenced by PAM50 molecular subtype. EPB42 may be of relevance to initiation, maintenance or progression of cancers of the female breast.


2019 ◽  
Vol 08 (02) ◽  
pp. 5-16
Author(s):  
Engin Altintas ◽  
Serap Yalin ◽  
Orhan Sezgin ◽  
Enver Ucbilek ◽  
Anil Tombak ◽  
...  

2018 ◽  
Vol 96 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Feng Dong ◽  
Tingting Liu ◽  
Hao Jin ◽  
Wenbo Wang

Epithelial-to-mesenchymal transition is a cellular process associated with cancer invasion and metastasis. However, the antimetastatic effects of chimaphilin remain elusive. In this study, we attempted to investigate the potential use of chimaphilin as an inhibitor of TGF-β1-induced epithelial-to-mesenchymal transition in U2OS cells. We found that TGF-β1 induced epithelial-to-mesenchymal transition to promote U2OS cell invasion and metastasis. Western blotting demonstrated that chimaphilin inhibited U2OS cell invasion and migration, increased the expression of the epithelial phenotype marker E-cadherin, repressed the expression of the mesenchymal phenotype marker vimentin, as well as decreased the level of epithelial-to-mesenchymal-inducing transcription factors Snail1 and Slug during the initiation of TGF-β1-induced epithelial-to-mesenchymal transition. In this study, we revealed that chimaphilin up-regulated the E-cadherin expression level and inhibited the production of vimentin, Snail1, and Slug in TGF-β1-induced U2OS cells by blocking PI-3K/Akt and ERK 1/2 signaling pathway. Additionally, the TGF-β1-mediated phosphorylated levels of Smad2/3 were inhibited by chimaphilin pretreatment. Above all, we conclude that chimaphilin represents an effective inhibitor of the metastatic potential of U2OS cells through suppression of TGF-β1-induced epithelial-to-mesenchymal transition.


1989 ◽  
Vol 78 (7) ◽  
pp. 990-991 ◽  
Author(s):  
Hiroyuki ITO ◽  
Kenji IZUHARA ◽  
Eisuke YOKOTA ◽  
Shuji NAKANO ◽  
Kazuma FUJIMOTO ◽  
...  

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