scholarly journals Nonlocal adhesion models for two cancer cell phenotypes in a multidimensional bounded domain

Author(s):  
Jaewook Ahn ◽  
Myeongju Chae ◽  
Jihoon Lee
2021 ◽  
Vol 1 (19) ◽  
pp. 86-88
Author(s):  
A.V. Grinchenko ◽  
A. Kriegsheim ◽  
N.A. Shved ◽  
A.E. Egorova ◽  
D.V. Ilyaskina ◽  
...  

A novel C1qDC bivalve protein from the bivalve Modiolus kurilensis (MkC1qDC-1) was identified, isolated and characterized. MkC1qDC-1 demonstrated the inhibition of HeLa cell proliferation and recognition of some cancer cell phenotypes in comparative analysis on several cell lines, suggesting biomedical potential of this protein.


2017 ◽  
Vol 58 (2) ◽  
pp. 84-98 ◽  
Author(s):  
Jennifer L. Illuzzi ◽  
Daniel R. McNeill ◽  
Paul Bastian ◽  
Boris Brenerman ◽  
Robert Wersto ◽  
...  
Keyword(s):  

2017 ◽  
Vol 108 (8) ◽  
pp. 1612-1619 ◽  
Author(s):  
Natalie Schudrowitz ◽  
Satoshi Takagi ◽  
Gary M. Wessel ◽  
Mamiko Yajima
Keyword(s):  

2018 ◽  
Vol 46 (5) ◽  
pp. 1137-1146 ◽  
Author(s):  
Arash Latifkar ◽  
Richard A. Cerione ◽  
Marc A. Antonyak

Tumor cells interact with each other, and their surroundings, using a variety of mechanisms to promote virtually all aspects of cancer progression. One such form of intercellular communication that has been attracting considerable attention from the cancer community and the pharmaceutical industry in recent years involves the ability of cancer cells to generate multiple distinct types of non-classical secretory vesicles, generally referred to as extracellular vesicles (EVs). Microvesicles (MVs) represent one of the major classes of EVs and are formed as a result of the outward budding and fission of the plasma membrane. The other main class of EVs is exosomes, which are generated when multivesicular bodies fuse with the cell surface and release their contents into the extracellular space. Both MVs and exosomes have been shown to contain bioactive cargo, including proteins, metabolites, RNA transcripts, microRNAs, and DNA that can be transferred to other cancer cells and stimulate their growth, survival, and migration. However, cancer cell-derived EVs also play important roles in helping re-shape the tumor microenvironment to support tumor expansion and invasive activity, dampen immune responses, as well as enter the circulation to help promote metastatic spread. Here, we provide an overview of what is currently known regarding how the different classes of EVs are generated and contribute to various cancer cell phenotypes. Moreover, we highlight how some of the unique properties of EVs are being used for the development of novel diagnostic and clinical applications.


2020 ◽  
Author(s):  
Yudong Tian ◽  
Yanbin Guan ◽  
Yang Su ◽  
Tao Yang ◽  
Haizhou Yu

Abstract Background: We aimed to study the effects of lncRNA TRPM2-AS in bladder cancer (BLCA) by interacting with its downstream effectors miR-22-3p and GINS2 mRNA.Methods: Online bioinformatic tools were used to identify the key lncRNA, miRNA and mRNA of interest in BLCA. TRPM2-AS, miR-22-3p and GINS2 mRNA expression was measured by qRT-PCR in bladder tissues and selected cell lines. Subcellular localization of TRPM2-AS in T24 and 5637 cell lines was identified using a cellular fractionation method. Luciferase reporter assay, RIP assay and RNA pull-down assay were employed to validate the direct binding relationship between TRPM2-AS, miR-22-3p and GINS2 mRNA. Cell viability, proliferation and apoptosis were measured by a series of cell functional experiments in T24 and 5637 cells.Results: TRPM2-AS was primarily located in cell cytoplasm and significantly up-regulated in BLCA tissues and cell lines. TRPM2-AS knockdown significantly inhibited cell viability and proliferation, but promoted cell apoptosis. miR-22-3p, a significant downstream target of TRPM2-AS, showed a lower expression level in BLCA tissues and cell lines. miR-22-3p inhibition resulted in a significant enhancement of BLCA cancer cell phenotypes. Lastly, GINS2 mRNA was a downstream target of miR-22-3p, and was significantly up-regulated in BLCA. The knockdown of GINS2 led to a significant suppression of BLCA cancer cell phenotypes.Conclusions: TRPM2-AS was a tumor promoter and fulfilling its role through binding to miR-22-3p to increase GINS2 expression. This novel interactome in BLCA might become a new therapy in BLCA.


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