scholarly journals CBX7 binds the E-box to inhibit TWIST-1 function and inhibit tumorigenicity and metastatic potential

Oncogene ◽  
2020 ◽  
Vol 39 (20) ◽  
pp. 3965-3979 ◽  
Author(s):  
Juanni Li ◽  
Ayesha B. Alvero ◽  
Sudhakar Nuti ◽  
Roslyn Tedja ◽  
Cai M. Roberts ◽  
...  
Keyword(s):  
E Box ◽  
2020 ◽  
Author(s):  
Juanni Li ◽  
Ayesha B Alvero ◽  
Sudhakar Nuti ◽  
Roslyn Tedja ◽  
Cai M. Roberts ◽  
...  

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Min Soo Kim ◽  
Joon Jeong ◽  
Jeongbeob Seo ◽  
Hae-Suk Kim ◽  
Seong-Jin Kim ◽  
...  

Abstract Metastatic breast cancers are aggressive tumors associated with high levels of epithelial-mesenchymal transition (EMT) markers, activation of IL6/JAK2/STAT3 and PI3K/AKT pathways for cell growth, mobility, invasion, metastasis, and CSC status. We identified a new molecular and functional network present in metastasis that regulates and coordinates with TrkC. Inhibition of SOCS3-mediated JAK2 degradation by TrkC increases total JAK2/STAT3 expression, and then leads to upregulation of Twist-1 through activation of JAK2/STAT3 cascade. Also, TrkC increases secretion and expression of IL-6, suggesting that this autocrine loop generated by TrkC maintains the mesenchymal state by continued activation of the JAK2/STAT3 cascade and upregulation of Twist expression. Moreover, TrkC interacts with the c-Src/Jak2 complex, which increases Twist-1 and Twist-2 levels via regulation of JAK2/STAT3 activation and JAK2/STAT3 expression. Furthermore, TrkC enhances metastatic potential of breast cancer via induction of EMT by upregulating Twist-1 and Twist-2. Additionally, TrkC significantly enhances the ability of breast cancer cells to form pulmonary metastases and primary tumor formation. Unexpectedly, we found that TrkC expression and clinical breast tumor pathological phenotypes show significant correlation. These findings suggest that TrkC plays a central role in tumorigenicity, metastasis, and self-renewal traits of metastatic breast cancer.


2018 ◽  
Author(s):  
Min Soo Kim ◽  
Hyun Sook Lee ◽  
Yun Jae Kim ◽  
Sung Gyun Kang ◽  
Do Yup Lee ◽  
...  

AbstractThe loss of imprinting of MEST has been linked to certain types of cancer by promoter switching. However, MEST-mediated regulation of tumorigenicity and metastasis are yet to be understood. Herein, we reported that MEST is a key regulator of IL-6/JAK/STAT3/Twist-1 signal pathway-mediated tumor metastasis. Enhanced MEST expression is significantly associated with pathogenesis of breast cancer patients. Also, MEST induces metastatic potential of breast cancer through induction of the EMT-TFs-mediated EMT program. Moreover, MEST leads to Twist-1 induction by STAT3 activation and subsequently enables the induction of activation of the EMT program via the induction of STAT3 nuclear translocation. Furthermore, the c-terminal region of MEST was essential for STAT3 activation via the induction of JAK2/STAT3 complex formation. Finally, MEST significantly increases the breast cancer’s ability to metastasize from the mammary gland to the lung. These observations suggest that MEST is a promising target for intervention to prevent tumor metastasis.


Author(s):  
C.D. Bucana ◽  
R. Sanchez ◽  
R. Singh ◽  
I.J. Fidler

The purpose of this study was to demonstrate by ISH the presence of IL-8 mRNA, and by immunohistochemistry (IHC) the presence of the chemokine IL-8 and the distribution of infiltrating macrophages in subcutaneous melanomas in the same tumor. IL-8 is a multifunctional cytokine produced by melanoma cells, activated macrophages and monocytes and it has been shown to be a growth and angiogenic factor for tumor cells. More recently it was shown that constitutive expression of IL-8 correlated directly with metastatic potential of human melanoma cells in nude mice. IL-8 content of a solid tumor as determined by Western blot analysis does not take into account the contribution of macrophages. Previous studies showed that murine tumors contain many infiltrating cells interspersed among tumor cells whereas human tumors growing in nude mice exhibit macrophages at the periphery or between tumor islands. In this study we demonstrate the expression of IL-8 and the distribution of macrophages by immunoperoxidase assay and IL-8 mRNA by ISH.


2020 ◽  
Vol 17 (3) ◽  
pp. 355-374
Author(s):  
John D. Ayres

This article considers the working practices of British cinema's only major female film producer during the early-to-mid post-Second World War era, Betty E. Box (1915–99). Via reference to her extensive archive at the British Film Institute and the films Campbell's Kingdom (1957), The Wind Cannot Read (1958) and Hot Enough for June (1964), the article charts how Box initially envisaged multi-generational casting for roles that were eventually taken by long-term collaborator Dirk Bogarde. It considers the manner in which she approached the diplomatic complexities of location shooting, with particular focus on Ralph Thomas's military romance The Wind Cannot Read, the first British film to be shot in India for twenty years at the time of its production. The reasoning for Box's ongoing absence, as a female creative figure, from scholarship addressing British cinema, and film production more generally, will also be addressed.


2016 ◽  
Author(s):  
Terese Karlsson ◽  
Reshma Sundar ◽  
Anders Widmark ◽  
Marene Landstrom ◽  
Emma Persson

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