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Multifunctional Applications of Engineered Extracellular Vesicles in the Treatment of Cancer.
Abstract Extracellular vesicles (EVs) are key players of intercellular communication in physiological and pathological conditions. In cancer, EVs mediate complex signaling mechanisms between cancer cells and the tumor microenvironment, and can influence tumor progression and the response to existing therapies. Importantly, EVs can be loaded with therapeutic agents and modified to display tumor-targeting molecules. In the field of nanomedicine, EVs have been engineered to serve as therapeutic delivery vehicles for several anti-cancer agents, including antibodies, chemotherapy, compounds, CRISPR/Cas9 and siRNA. Nota...
Source: Endocrinology - January 7, 2021 Category: Endocrinology Authors: Kugeratski FG, McAndrews KM, Kalluri R Tags: Endocrinology Source Type: research

Non-canonical Notch Signaling Regulates Actin Remodeling in Cell Migration by Activating PI3K/AKT/Cdc42 Pathway
In conclusion, our research results indicate that DAPT activates PI3K/AKT/Cdc42 signaling by non-canonical Notch pathway, and the activated Cdc42 promotes the filopodia formation and inhibits lamellipodia assembly, resulting in reduced migration of breast cancer cells. The results imply that non-canonical Notch signaling may play a very important role in the rapid response of cells to the extracellular signals. Author Contributions LG, JD, and LL designed the study and wrote and revised the manuscript. LL and LZ performed most of the experiments and data analysis. SZ, X-YZ, P-XM, Y-DM, Y-YW, YC, S-JT, and Y-JZ assisted i...
Source: Frontiers in Pharmacology - April 15, 2019 Category: Drugs & Pharmacology Source Type: research

Complement C5b-9 and Cancer: Mechanisms of Cell Damage, Cancer Counteractions, and Approaches for Intervention
In conclusion, osmotic burst of inflated complement-damaged cells may occur, but these bursts are most likely a consequence of metabolic collapse of the cell rather than the cause of cell death. The Complement Cell Death Mediator: A Concerted Action of Toxic Moieties Membrane pores caused by complement were first visualized by electron microscopy on red blood cell membranes as large ring structures (22). Similar lesions were viewed on E. coli cell walls (23). Over the years, ample information on the fine ultrastructure of the MAC that can activate cell death has been gathered (24) and has been recently further examined (...
Source: Frontiers in Immunology - April 9, 2019 Category: Allergy & Immunology Source Type: research

LSC - 2017 - Re-education of tumor-associated macrophages by modulating histone deacetylases in lung cancer
Conclusions: Suppression of HDAC2 switches M2-like TAMs into M1-like phenotype and regulates tumor cell functions. Modulation of HDAC2 may provide a novel strategy for TAMs repolarization and cancer therapy.
Source: European Respiratory Journal - December 6, 2017 Category: Respiratory Medicine Authors: Zheng, X. Tags: Lung Cancer Source Type: research