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

2021 ◽  
Vol 72 (2) ◽  
Author(s):  
Jaewook Ahn ◽  
Myeongju Chae ◽  
Jihoon Lee
Keyword(s):  
Bounded Domain ◽  
Cancer Cell ◽  
Cell Phenotypes

Abstract 744: Progesterone receptors promote quiescence & ovarian cancer cell phenotypes via modulation of DREAM in p53-mutant fallopian tube models

2021 ◽  
Author(s):  
Laura J. Mauro ◽  
Megan I. Seibel ◽  
Caroline H. Diep ◽  
Angela Spartz ◽  
Carlos Perez Kerkvliet ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cell ◽  
Fallopian Tube ◽  
Ovarian Cancer Cell ◽  
Progesterone Receptors ◽  
Cell Phenotypes

A NOVEL C1Q DOMAIN-CONTAINING PROTEIN ISOLATED FROM THE MOLLUSK MODIOLUS KURILENSIS RECOGNIZING GLYCANS ENRICHED WITH ACIDIC GALACTANS AND MANNANS IS VERY PROSPECTIVE FOR BIOMEDICAL PURPOSES

2021 ◽  
Vol 1 (19) ◽  
pp. 86-88
Author(s):  
A.V. Grinchenko ◽  
A. Kriegsheim ◽  
N.A. Shved ◽  
A.E. Egorova ◽  
D.V. Ilyaskina ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Comparative Analysis ◽  
Hela Cell ◽  
Cell Lines ◽  
Cancer Cell ◽  
Modiolus Kurilensis ◽  
Cell Phenotypes ◽  
Biomedical Potential

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.

scholarly journals Tumor-associated APE1 variant exhibits reduced complementation efficiency but does not promote cancer cell phenotypes

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

scholarly journals Germline factor DDX 4 functions in blood‐derived cancer cell phenotypes

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

scholarly journals Probing the mechanisms of extracellular vesicle biogenesis and function in cancer

2018 ◽  
Vol 46 (5) ◽  
pp. 1137-1146 ◽  
Author(s):  
Arash Latifkar ◽  
Richard A. Cerione ◽  
Marc A. Antonyak
Keyword(s):  
Cancer Cells ◽  
Cancer Cell ◽  
Cancer Progression ◽  
Extracellular Vesicle ◽  
Rna Transcripts ◽  
Main Class ◽  
Vesicle Biogenesis ◽  
And Migration ◽  
And Function ◽  
Cell Phenotypes

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.

scholarly journals TRPM2-AS promotes bladder cancer-genesis by targeting miR-22-3p thus releasing GINS2 mRNA

2020 ◽  
Author(s):  
Yudong Tian ◽  
Yanbin Guan ◽  
Yang Su ◽  
Tao Yang ◽  
Haizhou Yu
Keyword(s):  
Bladder Cancer ◽  
Cell Viability ◽  
Cell Lines ◽  
Cancer Cell ◽  
Tumor Promoter ◽  
Luciferase Reporter ◽  
Downstream Target ◽  
Bioinformatic Tools ◽  
Direct Binding ◽  
Cell Phenotypes

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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