scholarly journals ESR Method in Monitoring of Nanoparticle Endocytosis in Cancer Cells

2020 ◽  
Vol 21 (12) ◽  
pp. 4388
Author(s):  
Ryszard Krzyminiewski ◽  
Bernadeta Dobosz ◽  
Bart Krist ◽  
Grzegorz Schroeder ◽  
Joanna Kurczewska ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Nitroxide Radical ◽  
Microvascular Endothelial Cells ◽  
Essential Factor ◽  
Cellular Processes ◽  
Spin Resonance ◽  
A Cell ◽  
Suitable Technique ◽  
Model Nanoparticles

Magnetic nanoparticles are extensively studied for their use in diagnostics and medical therapy. The behavior of nanoparticles after adding them to cell culture is an essential factor (i.e., whether they attach to a cell membrane or penetrate the membrane and enter into the cell). The present studies aimed to demonstrate the application of electron spin resonance (ESR) as a suitable technique for monitoring of nanoparticles entering into cells during the endocytosis process. The model nanoparticles were composed of magnetite iron (II, III) oxide core functionalized with organic unit containing nitroxide radical 4-hydroxy-TEMPO (TEMPOL). The research studies included breast cancer cells, as well as model yeast and human microvascular endothelial cells. The results confirmed that the ESR method is suitable for studying the endocytosis process of nanoparticles in the selected cells. It also allows for direct monitoring of radical cellular processes.

scholarly journals Trastuzumab Modulates the Protein Cargo of Extracellular Vesicles Released by ERBB2+ Breast Cancer Cells

Membranes ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. 199
Author(s):  
Silvia Marconi ◽  
Sara Santamaria ◽  
Martina Bartolucci ◽  
Sara Stigliani ◽  
Cinzia Aiello ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Extracellular Vesicles ◽  
Breast Cancer Cells ◽  
Culture Supernatant ◽  
High Resolution Mass Spectrometry ◽  
Recombinant Antibody ◽  
Target Cells ◽  
Cellular Processes ◽  
Erbb2 Signaling

Cancers overexpressing the ERBB2 oncogene are aggressive and associated with a poor prognosis. Trastuzumab is an ERBB2 specific recombinant antibody employed for the treatment of these diseases since it blocks ERBB2 signaling causing growth arrest and survival inhibition. While the effects of Trastuzumab on ERBB2 cancer cells are well known, those on the extracellular vesicles (EVs) released from these cells are scarce. This study focused on ERBB2+ breast cancer cells and aimed to establish what type of EVs they release and whether Trastuzumab affects their morphology and molecular composition. To these aims, we performed immunoelectron microscopy, immunoblot, and high-resolution mass spectrometry analyses on EVs purified by differential centrifugation of culture supernatant. Here, we show that EVs released from ERBB2+ breast cancer cells are polymorphic in size and appearance and that ERBB2 is preferentially associated with large (120 nm) EVs. Moreover, we report that Trastuzumab (Tz) induces the expression of a specific glycosylated 50 kDa isoform of the CD63 tetraspanin and modulates the expression of 51 EVs proteins, including TOP1. Because these proteins are functionally associated with organelle organization, cytokinesis, and response to lipids, we suggest that Tz may influence these cellular processes in target cells at distant sites via modified EVs.

scholarly journals Protein Disulphide Isomerase A1 Is Involved in the Regulation of Breast Cancer Cell Adhesion and Transmigration via Lung Microvascular Endothelial Cells

Cancers ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 2850
Author(s):  
Marta Stojak ◽  
Magdalena Milczarek ◽  
Anna Kurpinska ◽  
Joanna Suraj-Prazmowska ◽  
Patrycja Kaczara ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Endothelial Cells ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Breast Cancer Cells ◽  
Transendothelial Migration ◽  
Microvascular Endothelial Cells ◽  
Protein Disulphide Isomerase ◽  
Cellular Bioenergetics ◽  
Microvascular Endothelial

Cancer cell cross-talk with the host endothelium plays a crucial role in metastasis, but the underlying mechanisms are still not fully understood. We studied the involvement of protein disulphide isomerase A1 (PDIA1) in human breast cancer cell (MCF-7 and MDA-MB-231) adhesion and transendothelial migration. For comparison, the role of PDIA1 in proliferation, migration, cell cycle and apoptosis was also assessed. Pharmacological inhibitor, bepristat 2a and PDIA1 silencing were used to inhibit PDIA1. Inhibition of PDIA1 by bepristat 2a markedly decreased the adhesion of breast cancer cells to collagen type I, fibronectin and human lung microvascular endothelial cells. Transendothelial migration of breast cancer cells across the endothelial monolayer was also inhibited by bepristat 2a, an effect not associated with changes in ICAM-1 expression or changes in cellular bioenergetics. The silencing of PDIA1 produced less pronounced anti-adhesive effects. However, inhibiting extracellular free thiols by non-penetrating blocker p-chloromercuribenzene sulphonate substantially inhibited adhesion. Using a proteomic approach, we identified that β1 and α2 integrins were the most abundant among all integrins in breast cancer cells as well as in lung microvascular endothelial cells, suggesting that integrins could represent a target for PDIA1. In conclusion, extracellular PDIA1 plays a major role in regulating the adhesion of cancer cells and their transendothelial migration, in addition to regulating cell cycle and caspase 3/7 activation by intracellular PDIA1. PDIA1-dependent regulation of cancer–endothelial cell interactions involves disulphide exchange and most likely integrin activation but is not mediated by the regulation of ICAM-1 expression or changes in cellular bioenergetics in breast cancer or endothelial cells.

scholarly journals A role for PVRL4-driven cell–cell interactions in tumorigenesis

eLife ◽  
2013 ◽  
Vol 2 ◽  
Author(s):  
Natalya N Pavlova ◽  
Christian Pallasch ◽  
Andrew EH Elia ◽  
Christian J Braun ◽  
Thomas F Westbrook ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Cell Adhesion Molecule ◽  
Cell Attachment ◽  
Poliovirus Receptor ◽  
Integrin Β4 ◽  
Growth Constraints ◽  
A Cell ◽  
Novel Strategy

During all stages of tumor progression, cancer cells are subjected to inappropriate extracellular matrix environments and must undergo adaptive changes in order to evade growth constraints associated with the loss of matrix attachment. A gain of function screen for genes that enable proliferation independently of matrix anchorage identified a cell adhesion molecule PVRL4 (poliovirus-receptor-like 4), also known as Nectin-4. PVRL4 promotes anchorage-independence by driving cell-to-cell attachment and matrix-independent integrin β4/SHP-2/c-Src activation. Solid tumors frequently have copy number gains of the PVRL4 locus and some have focal amplifications. We demonstrate that the transformation of breast cancer cells is dependent on PVRL4. Furthermore, growth of orthotopically implanted tumors in vivo is inhibited by blocking PVRL4-driven cell-to-cell attachment with monoclonal antibodies, demonstrating a novel strategy for targeted therapy of cancer.

scholarly journals Preparation of chitosan-Epigallocatechin-3-O-gallate nanoparticles and their inhibitory effect on the growth of breast cancer cells

2018 ◽  
Vol 11 (04) ◽  
pp. 1850018 ◽  
Author(s):  
Yingyi Liu ◽  
Siyi Hu ◽  
Yueshu Feng ◽  
Peng Zou ◽  
Yue Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Drug Carrier ◽  
Scratch Test ◽  
Inhibitory Effect ◽  
Inhibition Rate ◽  
Carrier System ◽  
A Cell ◽  
Drug Carrier System

In this paper, we prepared the nanoparticle drug carrier system between nanoparticles — chitosan and Epigallocatechin-3-O-gallate (EGCG) for breast cancer cell inhibiting application. For this drug carrier system, chitosan acts as a carrier and EGCG as a drug. Which were systematically characterized and thoroughly evaluated in terms of their inhibition rate and biocompatibility. We also did a cell scratch test and the result indicated that the chitosan-EGCG nanoparticles have inhibitory effect on the growth of breast cancer cells. The inhibition rate could reach up to 21.91%. This work revealed that the modification of nanoparticles paved a way for specific biomedical applications.

scholarly journals Trastuzumab Modulates the Protein Cargo of Extracellular Vesicles Released by ERBB2+ Breast Cancer Cells

2021 ◽  
Author(s):  
Silvia Marconi ◽  
Sara Santamaria ◽  
Martina Bertolucci ◽  
Sara Stigliani ◽  
Cinzia Aiello ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Extracellular Vesicles ◽  
Breast Cancer Cells ◽  
Culture Supernatant ◽  
High Resolution Mass Spectrometry ◽  
Recombinant Antibody ◽  
Target Cells ◽  
Cellular Processes ◽  
Erbb2 Signaling

Cancers overexpressing the ERBB2 oncogene are aggressive and associated with a poor prognosis. Trastuzumab is a ERBB2 specific recombinant antibody employed for the treatment of these diseases since it blocks ERBB2 signaling causing growth arrest and survival inhibition. While the effects of Trastuzumab on ERBB2 cancer cells are well known, those on the extracellular vesicles released from these cells are scarce. This study focused on ERBB2+ breast cancer cells and aimed to establish what type of EVs they release and whether Trastuzumab affects their morphology and molecular composition. To these aims, we performed immunoelectron microscopy, immunoblot, and high-resolution mass spectrometry analyses on EVs purified by differential centrifugation of culture supernatant. Here we show that EVs released from ERBB2+ breast cancer cells are polymorphic in size and appearance, and that ERBB2 is preferentially associated with large (120 nm) EVs. Moreover, we report that Tz induces the expression of a specific glycosylated 50 kDa isoform of the CD63 tetraspanin and modulates the expression of 51 EVs proteins, including TOP1. As these proteins are functionally associated with organelle organization, cytokinesis, and response to lipids, we suggest that Tz may influence these cellular processes in target cells at distant sites via modified EVs.

Wheat germ agglutinin modified magnetic iron oxide nanocomplex as a cell membrane specific receptor target material for killing breast cancer cells

2018 ◽  
Vol 6 (36) ◽  
pp. 5729-5737 ◽  
Author(s):  
Aekta Upadhyay ◽  
Ravinder Kandi ◽  
Chebrolu Pulla Rao
Keyword(s):  
Breast Cancer ◽  
Iron Oxide ◽  
Cancer Cells ◽  
Wheat Germ Agglutinin ◽  
Breast Cancer Cells ◽  
Wheat Germ ◽  
Target Material ◽  
Magnetic Iron Oxide Nanoparticles ◽  
Magnetic Iron Oxide ◽  
A Cell

The magnetic iron oxide nanoparticles were coated with a fluorescent torch and were further tagged with wheat germ agglutinin so as to direct the resulting nanocomplex selectively towards breast cancer cells in order to deliver the drug.

scholarly journals A Cell-Permeant Amiloride Derivative Induces Caspase-Independent, AIF-Mediated Programmed Necrotic Death of Breast Cancer Cells

PLoS ONE ◽  
2013 ◽  
Vol 8 (4) ◽  
pp. e63038 ◽  
Author(s):  
Leonardo J. Leon ◽  
Nagarekha Pasupuleti ◽  
Fredric Gorin ◽  
Kermit L. Carraway
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
A Cell

scholarly journals Breast Cancer Stem Cells Survive Periods of Farnesyl-Transferase Inhibitor-Induced Dormancy by Undergoing Autophagy

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Moumita Chaterjee ◽  
Kenneth L. van Golen
Keyword(s):  
Breast Cancer ◽  
Stem Cell ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Metastatic Potential ◽  
Stem Cell Markers ◽  
Farnesyl Transferase ◽  
Differentiated Cells ◽  
A Cell ◽  
Cluster Of Differentiation

A cancer stem cell has been defined as a cell within a tumor that possesses the capacity to self-renew and to cause the heterogeneous lineages of cancer cells that comprise the tumor. These tumor-forming cells could hypothetically originate from stem, progenitor, or differentiated cells. Previously, we have shown that breast cancer cells with low metastatic potential can be induced into a reversible state of dormancy by farnesyl transferase inhibitors (FTIs). Dormancy was induced by changes in RhoA and RhoC GTPases. Specifically, RhoA was found to be hypoactivated while RhoC was hyperactivated. In the current study we demonstrate that these dormant cells also express certain known stem cell markers such as aldehyde dehydrogenase I (ALDHI) and cluster of differentiation 44 (CD44). We also show that autophagy markers Atg5, Atg12, and LC3-B are expressed in these dormant stem cell-like breast cancer cells. Inhibiting autophagy by inhibitor 3-methyladenine (3-MA) blocked the process of autophagy reversing the dormant phenotype. Further, we show that c-jun NH2 terminal kinase (JNK/SAPK) is upregulated in these dormant stem cell-like breast cancer cells and is responsible for increasing autophagy.

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