scholarly journals LINC00511 contributes to glioblastoma tumorigenesis and epithelial‐mesenchymal transition via LINC00511/miR‐524‐5p/YB1/ZEB1 positive feedback loop

2019 ◽  
Vol 24 (2) ◽  
pp. 1474-1487 ◽  
Author(s):  
Xiaoliu Du ◽  
Yiming Tu ◽  
Shuang Liu ◽  
Pengzhan Zhao ◽  
Zhongyuan Bao ◽  
...  
Keyword(s):  
Positive Feedback ◽  
Feedback Loop ◽  
Epithelial Mesenchymal Transition ◽  
Positive Feedback Loop ◽  
Mesenchymal Transition

scholarly journals Persistent activation of STAT 3 by PIM 2‐driven positive feedback loop for epithelial‐mesenchymal transition in breast cancer

2015 ◽  
Vol 106 (6) ◽  
pp. 718-725 ◽  
Author(s):  
Nizam Uddin ◽  
Rae‐Kwon Kim ◽  
Ki‐Chun Yoo ◽  
Young‐Heon Kim ◽  
Yan‐Hong Cui ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Positive Feedback ◽  
Feedback Loop ◽  
Epithelial Mesenchymal Transition ◽  
Positive Feedback Loop ◽  
Mesenchymal Transition

scholarly journals AKR1B1 promotes basal-like breast cancer progression by a positive feedback loop that activates the EMT program

2017 ◽  
Vol 214 (4) ◽  
pp. 1065-1079 ◽  
Author(s):  
Xuebiao Wu ◽  
Xiaoli Li ◽  
Qiang Fu ◽  
Qianhua Cao ◽  
Xingyu Chen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Progression ◽  
Positive Feedback ◽  
Poor Prognosis ◽  
Feedback Loop ◽  
Epithelial Mesenchymal Transition ◽  
Breast Cancer Patients ◽  
Positive Feedback Loop ◽  
Mesenchymal Transition ◽  
Basal Like Breast Cancer

Basal-like breast cancer (BLBC) is associated with high-grade, distant metastasis and poor prognosis. Elucidating the determinants of aggressiveness in BLBC may facilitate the development of novel interventions for this challenging disease. In this study, we show that aldo-keto reductase 1 member B1 (AKR1B1) overexpression highly correlates with BLBC and predicts poor prognosis in breast cancer patients. Mechanistically, Twist2 transcriptionally induces AKR1B1 expression, leading to nuclear factor κB (NF-κB) activation. In turn, NF-κB up-regulates Twist2 expression, thereby fulfilling a positive feedback loop that activates the epithelial–mesenchymal transition program and enhances cancer stem cell (CSC)–like properties in BLBC. AKR1B1 expression promotes, whereas AKR1B1 knockdown inhibits, tumorigenicity and metastasis. Importantly, epalrestat, an AKR1B1 inhibitor that has been approved for the treatment of diabetic complications, significantly suppresses CSC properties, tumorigenicity, and metastasis of BLBC cells. Together, our study identifies AKR1B1 as a key modulator of tumor aggressiveness and suggests that pharmacologic inhibition of AKR1B1 has the potential to become a valuable therapeutic strategy for BLBC.

scholarly journals A theoretical approach to coupling the epithelial-mesenchymal transition (EMT) to extracellular matrix (ECM) stiffness via LOXL2

2021 ◽  
Author(s):  
Youyuan Deng ◽  
Priyanka Chakraborty ◽  
Mohit Kumar Jolly ◽  
Herbert Levine
Keyword(s):  
Extracellular Matrix ◽  
Cancer Progression ◽  
Positive Feedback ◽  
Feedback Loop ◽  
Epithelial Mesenchymal Transition ◽  
Critical Role ◽  
Cross Linking ◽  
Positive Feedback Loop ◽  
Mesenchymal Transition ◽  
The Impact

AbstractThe epithelial-mesenchymal transition (EMT) plays a critical role in cancer progression, being responsible in many cases for the onset of the metastatic cascade and being integral in the ability of cells to resist drug treatment. Most studies of EMT focus on its induction via chemical signals such as TGF-β or Notch ligands, but it has become increasingly clear that biomechanical features of the microenvironment such as ECM (extracellular matrix) stiffness can be equally important. Here, we introduce a coupled feedback loop connecting stiffness to the EMT transcription factor ZEB1, which acts via increasing the secretion of LOXL2 that leads to increased cross-linking of collagen fibers in the ECM. This increased cross-linking can effectively increase ECM stiffness and increase ZEB1 levels, thus setting a positive feedback loop between ZEB1 and ECM stiffness. To investigate the impact of this non-cell-autonomous effect, we introduce a computational approach capable of connecting LOXL2 concentration to increased stiffness and thereby to higher ZEB1 levels. Our results indicate that this positive feedback loop, once activated, can effectively lock the cells in a mesenchymal state.

scholarly journals A positive feedback loop between TAZ and miR-942-3p modulates proliferation, angiogenesis, epithelial-mesenchymal transition process, glycometabolism and ROS homeostasis in human bladder cancer

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Feifan Wang ◽  
Mengjing Fan ◽  
Xuejian Zhou ◽  
Yanlan Yu ◽  
Yueshu Cai ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cancer Cells ◽  
Positive Feedback ◽  
Feedback Loop ◽  
Epithelial Mesenchymal Transition ◽  
Biological Functions ◽  
Positive Feedback Loop ◽  
Mesenchymal Transition ◽  
Qrt Pcr ◽  
Bladder Cancer Cells

Abstract Background Transcriptional coactivator with PDZ-binding motif (TAZ) has been reported to be involved in tumor progression, angiogenesis, epithelial-mesenchymal transition (EMT), glycometabolic modulation and reactive oxygen species (ROS) buildup. Herein, the underlying molecular mechanisms of the TAZ-induced biological effects in bladder cancer were discovered. Methods qRT-PCR, western blotting and immunohistochemistry were performed to determine the levels of TAZ in bladder cancer cells and tissues. CCK-8, colony formation, tube formation, wound healing and Transwell assays and flow cytometry were used to evaluate the biological functions of TAZ, miR-942-3p and growth arrest-specific 1 (GAS1). QRT-PCR and western blotting were used to determine the expression levels of related genes. Chromatin immunoprecipitation and a dual-luciferase reporter assay were performed to confirm the interaction between TAZ and miR-942. In vivo tumorigenesis and colorimetric glycolytic assays were also conducted. Results We confirmed the upregulation and vital roles of TAZ in bladder cancer. TAZ-induced upregulation of miR-942-3p expression amplified upstream signaling by inhibiting the expression of large tumor suppressor 2 (LATS2, a TAZ inhibitor). MiR-942-3p attenuated the impacts on cell proliferation, angiogenesis, EMT, glycolysis and ROS levels induced by TAZ knockdown. Furthermore, miR-942-3p restrained the expression of GAS1 to modulate biological behaviors. Conclusion Our study identified a novel positive feedback loop between TAZ and miR-942-3p that regulates biological functions in bladder cancer cells via GAS1 expression and illustrated that TAZ, miR-942-3p and GAS1 might be potential therapeutic targets for bladder cancer treatment.

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