scholarly journals Control of Cytoskeletal Dynamics in Cancer through a Combination of Cytoskeletal Components

2022 ◽  
Author(s):  
Ban Hussein Alwash ◽  
Rawan Asaad Jaber Al-Rubaye ◽  
Mustafa Mohammad Alaaraj ◽  
Anwar Yahya Ebrahim
Keyword(s):  
Epithelial Mesenchymal Transition ◽  
S100 Protein ◽  
Tumor Development ◽  
Dynamic Structure ◽  
Cytoskeletal Proteins ◽  
S100a4 Protein ◽  
Invasion And Migration ◽  
Cytoskeletal Dynamics ◽  
Biological Target ◽  
And Migration

The dynamic alterations in the cytoskeletal components actin and intermediate, etc. filaments are required for cell invasion and migration. The actin cytoskeleton is a highly dynamic structure that is governed by a delicate balance of actin filament formation and disassembly. To controlling the activities of key components of the epithelial mesenchymal transition (EMT) could be a viable solution to metastasis. Bioinformatics technologies also allow researchers to investigate the consequences of synthetic mutations or naturally occurring variations of these cytoskeletal proteins. S100A4 is S100 protein family member that interact with a variety of biological target. In study has shown that S100A4 interacts with the tumor suppressor protein p53, indicating that S100A4 may have additional roles in tumor development. The S100A4 and p53 interaction increases after inhibition of MDM2-dependent p53 degradation using Nutlin-3A. The main goal of this research was control of cytoskeletal dynamics in cancer through a combination of, actin and S100A4 protein. The investigate the molecular mechanism behind S100A4 function in (EMT) and indicating that S100A4 is promoting p53 degradation. Understanding the signaling pathways involved would provide a better understanding of the changes that occur during metastasis, which will eventually lead to the identification of proteins that can be targeted for treatment, resulting in lower mortality.

scholarly journals EMT Participates in the Regulation of Exosomes Secretion and Function in Esophageal Cancer Cells

2021 ◽  
Vol 20 ◽  
pp. 153303382110330
Author(s):  
Chuangui Chen ◽  
Zhao Ma ◽  
Hongjing Jiang
Keyword(s):  
Esophageal Cancer ◽  
Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Promoting Effect ◽  
Migration Ability ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
And Migration ◽  
And Function ◽  
Esophageal Cancer Cells

Epithelial-mesenchymal transition (EMT) is a key step in tumor invasion and distant metastasis. Abundant evidence has documented that exosomes can mediate EMT of tumor cells and endow them with the ability of invasion and migration. However, there are few studies focusing on whether EMT can reverse the secretion of exosomes. In this study, 2 esophageal cancer cells (FLO-1 and SK-GT-4) were selected to compare the migration ability and EMT activation, and to further analyze the secretion ability of exosomes of the 2 cell lines. According to the results, inhibited activation of EMT in FLO-1 cells with relatively high migration ability could effectively reduce the secretion of exosomes. Besides, in SK-GT-4 cells, EMT activation induced by TGF-β could promote the secretion of exosomes. FLO-1 cell derived exosomes exhibited a paracrine effect of promoting the migration of SK-GT-4 cells, and the use of EMT inhibitors could weaken this ability. Furthermore, inhibition of EMT could change the relative content of some miRNAs in exosomes, with a particularly significant downregulation in the expression of miR-196-5p, miR-21-5p and miR-194-5p. Significantly, artificial transfection of the 3 miRNAs into exosomes by electroporation resulted in the recovery of migration-promoting effect of exosomes. Subsequent experiments further revealed that the effect of EMT on these miRNAs could be explained by the intracellular transcription level or the specific sorting mechanism of exosomes. To sum up, our study undoubtedly reveals that EMT has a regulatory effect on exosomes in the quantity and contents in esophageal cancer cells. Significantly, findings in our study provide experimental evidence for the interaction of EMT with the secretion and sorting pathway of exosomes, and also give a new direction for the further study of tumor metastasis.

scholarly journals Benzotriazole Enhances Cell Invasive Potency in Endometrial Carcinoma Through CTBP1-Mediated Epithelial-Mesenchymal Transition

2017 ◽  
Vol 44 (6) ◽  
pp. 2357-2367 ◽  
Author(s):  
Yiquan Wang ◽  
Chencheng Dai ◽  
Cheng Zhou ◽  
Wenqu Li ◽  
Yujia Qian ◽  
...  
Keyword(s):  
Endometrial Carcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Expression Patterns ◽  
Underlying Mechanism ◽  
Carcinoma Cells ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
Female Reproductive Health ◽  
Gene Microarray Analysis ◽  
And Migration

Background/Aims: Benzotriazole (BTR) and its derivatives, such as intermediates and UV stabilizers, are important man-made organic chemicals found in everyday life that have been recently identified as environmental toxins and a threat to female reproductive health. Previous studies have shown that BTR could act as a carcinogen by mimicking estrogen. Environmental estrogen mimics could promote the initiation and development of female cancers, such as endometrial carcinoma, a type of estrogenic-sensitive malignancy. However, there is little information on the relationship between BTR and endometrial carcinoma. In this study, we aimed to demonstrate the biological function of BTR in endometrial carcinoma and explored the underlying mechanism. Methods: The CCK-8 assay was performed to detect cell viability; transwell-filter assay was used to assess cell invasion; gene microarray analysis was employed to determine gene expression patterns in response to BTR treatment; western blotting and quantitative reverse transcription polymerase chain reaction (qRT-PCR) were carried out to detect the expression levels of BTR-related genes. Results: Our data showed that BTR could induce the invasion and migration of endometrial carcinoma cells (Ishikawa and HEC-1-B). In addition, BTR increased the expression level of CTBP1, which could enhance the epithelial-mesenchymal transition (EMT) in cancer cells. Moreover, CTBP1 silencing reversed the effect of BTR on EMT progression in endometrial carcinoma cells. Conclusion: This study indicates that BTR could act as a carcinogen to promote the development of endometrial carcinoma mainly through CTBP1-mediated EMT, which deserves more attention.

scholarly journals BK polyomavirus infection promotes growth and aggressiveness in bladder cancer

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Yigang Zeng ◽  
Jiajia Sun ◽  
Juan Bao ◽  
Tongyu Zhu
Keyword(s):  
Bladder Cancer ◽  
Signaling Pathway ◽  
Epithelial Mesenchymal Transition ◽  
Cell Model ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
Urothelial Carcinomas ◽  
Bk Polyomavirus ◽  
And Migration

Abstract Background Recent studies have confirmed the integration of the BK polyomavirus (BKPyV) gene into the cellular genome of urothelial carcinomas in transplant recipients, further confirming the correlation between BKPyV and urothelial carcinomas after transplantation. However, the role BKPyV infections play in the biological function of bladder cancer remains unclear. Methods We developed a BKPyV-infected bladder cancer cell model and a mice tumor model to discuss the role of BKPyV infections. Results Our research proves that BKPyV infections promote the proliferation, invasion and migration of bladder cancer cells, while the activation of β-catenin signaling pathway is one of its mediation mechanisms. Conclusions We first described BKPyV infection promotes the proliferation, invasion and migration of bladder cancer. We verified the role of β-catenin signaling pathway and Epithelial-Mesenchymal Transition effect in BKPyV-infected bladder cancer. These results provide meaningful information towards the diagnosis and treatment of clinical bladder cancer.

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