Quantitative Localized Analysis Reveals Distinct Exosomal Protein-Specific Glycosignatures: Implications in Cancer Cell Subtyping, Exosome Biogenesis, and Function

2020 ◽  
Vol 142 (16) ◽  
pp. 7404-7412
Author(s):  
Yuna Guo ◽  
Jing Tao ◽  
Yiran Li ◽  
Yimei Feng ◽  
Huangxian Ju ◽  
...  
Keyword(s):  
Cancer Cell ◽  
Exosome Biogenesis ◽  
Localized Analysis ◽  
And Function

scholarly journals The expression and function of toll-like receptors (TLRs) in ovarian cancer cell lines

2015 ◽  
Vol 3 (S2) ◽  
Author(s):  
Shin-Wha Lee ◽  
In-Kyung Lee ◽  
Sumin Kim ◽  
Sang-Eun Lee ◽  
Ha-Young Lee ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Ovarian Cancer Cell ◽  
Cancer Cell Lines ◽  
Toll Like Receptors ◽  
Ovarian Cancer Cell Lines ◽  
And Function

scholarly journals Conserved tryptophan mutation disrupts structure and function of immunoglobulin domain revealing unusual tyrosine fluorescence

2020 ◽  
Author(s):  
Ravi Vattepu ◽  
Rachel A. Klausmeyer ◽  
Allan Ayella ◽  
Rahul Yadav ◽  
Joseph T. Dille ◽  
...  
Keyword(s):  
Cell Line ◽  
Domain Structure ◽  
Cancer Cell ◽  
Cancer Cell Line ◽  
Actin Binding ◽  
Structure Stability ◽  
Hydrophobic Core ◽  
Tyrosine Fluorescence ◽  
And Function ◽  
Ig Domain

ABSTRACTImmunoglobulin (Ig) domains are the most prevalent protein domain structure and share a highly conserved folding pattern; however, this structural family of proteins is also the most diverse in terms of biological roles and tissue expression. Ig domains vary significantly in amino acid sequence but share a highly conserved tryptophan in the hydrophobic core of this beta-stranded protein. Palladin is an actin binding and bundling protein that has five Ig domains and plays an important role in normal cell adhesion and motility. Mutation of the core tryptophan in one Ig domain of palladin has been identified in a pancreatic cancer cell line, suggesting a crucial role for this sole tryptophan in palladin Ig domain structure, stability, and function. We found that actin binding and bundling was not completely abolished with removal of this tryptophan despite a partially unfolded structure and significantly reduced stability of the mutant Ig domain as shown by circular dichroism investigations. In addition, this mutant palladin domain displays a tryptophan-like fluorescence attributed to an anomalous tyrosine emission at 345 nm. Our results indicate that this emission originates from a tyrosinate that may be formed in the excited ground state by proton transfer to a nearby glutamyl residue. Furthermore, this study emphasizes the importance of tryptophan in protein structural stability and illustrates how tyrosinate emission contributions may be overlooked during the interpretation of the fluorescence properties of proteins.SHORT ABSTRACTThis study explores the functional and structural consequences of a point mutation in palladin, an Ig domain protein first identified in a pancreatic tumor cancer cell line. While exploring the consequences of mutating this conserved tryptophan in the hydrophobic core of the most prevalent domain structure found in proteins, an anomalous tyrosine fluorescence phenomenon was exposed.

scholarly journals Breast cancer cell cyclooxygenase-2 expression alters extracellular matrix structure and function and numbers of cancer associated fibroblasts

Oncotarget ◽  
2017 ◽  
Vol 8 (11) ◽  
pp. 17981-17994 ◽  
Author(s):  
Balaji Krishnamachary ◽  
Ioannis Stasinopoulos ◽  
Samata Kakkad ◽  
Marie-France Penet ◽  
Desmond Jacob ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Extracellular Matrix ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Structure And Function ◽  
Cyclooxygenase 2 ◽  
Cancer Associated Fibroblasts ◽  
Matrix Structure ◽  
And Function

scholarly journals RASSF1A Suppresses Estrogen-Dependent Breast Cancer Cell Growth through Inhibition of the Yes-Associated Protein 1 (YAP1), Inhibition of the Forkhead Box Protein M1 (FOXM1), and Activation of Forkhead Box Transcription Factor 3A (FOXO3A)

Cancers ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2689
Author(s):  
Sven Roßwag ◽  
Gitta Thiede ◽  
Jonathan P. Sleeman ◽  
Sonja Thaler
Keyword(s):  
Breast Cancer ◽  
Transcription Factor ◽  
Cell Growth ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Cell Growth ◽  
Breast Cancer Cell Growth ◽  
Forkhead Box ◽  
Cancer Initiation ◽  
And Function

The estrogen receptor alpha (ERα) is expressed by the majority of breast cancers and plays an important role in breast cancer development and tumor outgrowth. Although ERα is well known to be a specific and efficient therapeutic target, the molecular mechanisms that are responsible for the control of ERα expression and function in the context of breast cancer initiation and progression are complex and not completely elucidated. In previous work, we have demonstrated that the tumor suppressor RASSF1A inhibits ERα expression and function in ERα-positive breast cancer cells through an AKT-dependent mechanism. Transcriptional activators such as forkhead box protein M1 (FOXM1) and forkhead transcription factor 3A (FOXO3A) and signaling pathways such as the Hippo pathway are also known to modulate ERα expression and activity. Here we report that RASSF1A acts as an inhibitor of ERα-driven breast cancer cell growth through a complex, hierarchically organized network that initially involves suppression of the Hippo effector Yes-associated protein 1 (YAP1), which is followed by inhibition of AKT1 activity, increased FOXO3A activity as well as a blockade of FOXM1 and ERα expression. Together our findings provide important new mechanistic insights into how the loss of RASSF1A contributes to ERα+ breast cancer initiation and progression.

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 Exosome biogenesis, secretion and function of exosomal miRNAs in skeletal muscle myogenesis

2020 ◽  
Vol 53 (7) ◽  
Author(s):  
Binglin Yue ◽  
Haiyan Yang ◽  
Jian Wang ◽  
Wenxiu Ru ◽  
Jiyao Wu ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exosome Biogenesis ◽  
Exosomal Mirnas ◽  
And Function

scholarly journals The Effects of 17β-estradiol on Mitochondrial Biogenesis and Function in Breast Cancer Cell Lines are Dependent on the ERα/ERβ Ratio

2012 ◽  
Vol 29 (1-2) ◽  
pp. 261-268 ◽  
Author(s):  
Jorge Sastre-Serra ◽  
Mercedes Nadal-Serrano ◽  
Daniel Gabriel Pons ◽  
Adamo Valle ◽  
Jordi Oliver ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Mitochondrial Biogenesis ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines ◽  
17Β Estradiol ◽  
And Function

scholarly journals circCOL1A1 Promotes the Progression of Gastric Cancer Cells through Sponging miR-145 to Enhance RABL3 Expression

2021 ◽  
Vol 2021 ◽  
pp. 1-20
Author(s):  
Yue Ma ◽  
Yanyi Ren ◽  
Huitao Wen ◽  
Chengcheng Cui
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Circular Rna ◽  
Migration And Invasion ◽  
Gastric Cancer Cells ◽  
Gastric Cancer Cell Lines ◽  
Microrna Sponge ◽  
And Function

Circular RNA has been reported to be a new noncoding RNA which plays important roles in tumor progression. One of the most common functions of circular RNA is to regulate microRNA expression by acting as a microRNA sponge. However, the circular RNA expression profile and function remain mostly unclear in gastric cancer. In the study, we explored the expression and function of circCOL1A1 (hsa_circ_0044556) in gastric cancer. We performed RT-PCR with divergent primers, mRNA stability assay, and RNase R digestion assay to characterize circCOL1A1 in gastric cancer cell lines. qRT-PCR was applied to detect the level of circCOL1A1 in both gastric cancer cell lines and tissues. Gain- and loss-of-function studies were carried out to detect the influence of circCOL1A1 on gastric cancer cells by performing CCK8, migration, and invasion assays. The regulation of the downstream genes was identified by qRT-PCR, western blot assay, dual luciferase assay, and RNA pull-down assay. The results showed that circCOL1A1 was highly expressed in both gastric cancer cells and tissues. Silence of circCOL1A1 inhibited the proliferation, migration, and invasion of gastric cancer cells. circCOL1A1 regulated the expression of miR-145 by acting as a microRNA sponge, and the influence of circCOL1A1 could be abrogated by miR-145 mimics. Our research shows that miR-145 plays its functions through targeting and regulating RABL3. Inhibition of circCOL1A1/miR-145/RABL3 could effectively suppress gastric cancer cell proliferation, migration, and invasion. circCOL1A1 also promote the transformation of M1 into M2 macrophage. Our study identified circCOL1A1 as a novel oncogenic circRNA and will provide more information for gastric cancer therapy.

scholarly journals Glia-derived exosomal miR-274 targets Sprouty in trachea and synaptic boutons to modulate growth and responses to hypoxia

2019 ◽  
Vol 116 (49) ◽  
pp. 24651-24661 ◽  
Author(s):  
Yi-Wei Tsai ◽  
Hsin-Ho Sung ◽  
Jian-Chiuan Li ◽  
Chun-Yen Yeh ◽  
Pei-Yi Chen ◽  
...  
Keyword(s):  
Cell Growth ◽  
Target Cell ◽  
Target Gene ◽  
Mapk Signaling ◽  
Target Cells ◽  
Null Mutant ◽  
Specific Expression ◽  
Exosome Biogenesis ◽  
Synaptic Boutons ◽  
And Function

Secreted exosomal microRNAs (miRNAs) mediate interorgan/tissue communications by modulating target gene expression, thereby regulating developmental and physiological functions. However, the source, route, and function in target cells have not been formally established for specific miRNAs. Here, we show that glial miR-274 non-cell-autonomously modulates the growth of synaptic boutons and tracheal branches. Whereas the precursor form of miR-274 is expressed in glia, the mature form of miR-274 distributes broadly, including in synaptic boutons, muscle cells, and tracheal cells. Mature miR-274 is secreted from glia to the circulating hemolymph as an exosomal cargo, a process requiring ESCRT components in exosome biogenesis and Rab11 and Syx1A in exosome release. We further show that miR-274 can function in the neurons or tracheal cells to modulate the growth of synaptic boutons and tracheal branches, respectively. Also, miR-274 uptake into the target cells by AP-2–dependent mechanisms modulates target cell growth. In the target cells, miR-274 down-regulates Sprouty (Sty) through a targeting sequence at the sty 3′ untranslated region, thereby enhancing MAPK signaling and promoting cell growth. miR-274 expressed in glia of an mir-274 null mutant is released as an exosomal cargo in the circulating hemolymph, and such glial-specific expression resets normal levels of Sty and MAPK signaling and modulates target cell growth. mir-274 mutant larvae are hypersensitive to hypoxia, which is suppressed by miR-274 expression in glia or by increasing tracheal branches. Thus, glia-derived miR-274 coordinates growth of synaptic boutons and tracheal branches to modulate larval hypoxia responses.

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