scholarly journals Exosomes in Cancer Diagnosis and Radiation Therapy

2021 ◽  
Author(s):  
Ai Nakaoka ◽  
Kana Kobayashi ◽  
Mennaallah Hassan ◽  
Ryohei Sasaki
Keyword(s):  
Radiation Therapy ◽  
Cancer Cells ◽  
Vascular Endothelial Cells ◽  
Strand Break ◽  
Current Evidence ◽  
Vascular Endothelial ◽  
Messenger Rnas ◽  
Normal Cells ◽  
Dna Double Strand Break ◽  
Repair Ability

Exosomes are a subgroup of extracellular vesicles that are released by all types of cells, including tumor cells, and mediate intercellular communication via the transport of various intracellular components, including microRNAs, messenger RNAs, and proteins. Radiation produces reactive oxygen species and induces DNA double-strand break in cancer cells and normal cells. Cancer cells have severe damage and die by irradiation, but normal cells can keep proliferation with their high DNA repair ability. Irradiated cells generate communication signals and cause biological changes in neighboring or distant non-irradiated cells. This review outlines the role of exosomes in radiation therapy. In the tumor microenvironment, exosomes are considered to regulate cell survival, migration, and resistance to therapy by interacting with vascular endothelial cells and various types of immune cells. Nowadays, radiation therapy is typically combined with immunotherapy. Regulation of the activity of exosomes may overcome the problem of resistance to immunotherapy. Furthermore, exosomes can attenuate resistance to chemotherapy by transporting certain types of microRNA. The current evidence suggests that exosomes may be useful in the diagnosis and treatment of cancer in the future.

Quantification of DNA double-strand break induced by radiation in cervix cancer cells: in vitro study

2018 ◽  
Vol 18 (1) ◽  
pp. 52-54
Author(s):  
Sothing Vashum ◽  
Rabi Raja Singh I ◽  
Saikat Das ◽  
Mohammed Azharuddin KO ◽  
Prabhakaran Vasudevan
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Strand Break ◽  
Double Strand Break ◽  
Ionising Radiation ◽  
Dependent Manner ◽  
Survival Fraction ◽  
Dna Double Strand Break ◽  
Cervical Cancer Cells

AbstractAimDNA double-strand break (DSB) results in the phosphorylation of the protein, H.2AX histone. In this study, the effect of radiotherapy and chemotherapy on DNA DSB in cervical cancer cells is analysed by the phosphorylation of the protein.MethodsThe cervical cancer cells (HeLa cells) were cultured and exposed to ionising radiation. Radiation sensitivity was measured by clonogenic survival fraction after exposing to ionising radiation. Since the phosphorylation of H.2AX declines with time, the DNA damage was quantified at different time points: 1 hour, 3 hours and 1 week after exposed to the radiation. The analysis of γ-H.2AX was done by Western-blot technique. The protein expression was observed at different dose of radiation and combination of both radiation and paclitaxel.ResultsLow-dose hypersensitivity was observed. By 1 week after radiation at 0·5, 0·8 and 2 Gy, there was no expression of phosphorylated H.2AX. Previous experiments on the expression of phosphorylated H.2AX (γ-H.2AX) in terms of foci analysis was found to peak at 1 hour and subsequently decline with time. In cells treated with the DNA damaging agents, the expression of phosphorylated H.2AX decreases in a dose-dependent manner when treated with radiation alone. However, when combined with paclitaxel, at 0·5 Gy, the expression peaked and reduces at 0·8 Gy and slightly elevated at 2 Gy.FindingsIn this study, the peak phosphorylation was observed at 3 hour post irradiation indicating that DSBs are still left unrepaired.

scholarly journals DNA double-strand break repair efficiency in cancer cells exposed to laser-driven ultrashort electron beams

2021 ◽  
Author(s):  
Andreyan Osipov ◽  
Nelly Babayan ◽  
Natalia Vorobyeva ◽  
Bagrat Grigoryan ◽  
Anna Chigasova-Grekhova ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Electron Beams ◽  
Strand Break ◽  
Double Strand Break ◽  
Double Strand Break Repair ◽  
Dna Double Strand Break ◽  
Repair Efficiency ◽  
Break Repair

YAP Overexpression in Breast Cancer Cells Promotes Angiogenesis Through Activating Yap Signaling in Vascular Endothelial Cells

2020 ◽  
Author(s):  
Yu Yan ◽  
Qiang Song ◽  
Li Yao ◽  
Liang Zhao ◽  
Hui Cai
Keyword(s):  
Breast Cancer ◽  
Endothelial Cells ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Tumor Angiogenesis ◽  
Breast Cancer Cells ◽  
Vascular Endothelial Cells ◽  
Tissue Growth ◽  
Vascular Endothelial ◽  
Potential Marker

Abstract Background:The YAP signaling pathway is altered and implicated as oncogenic in human mammary cancers.However, roles of YAP signaling that regulate the breast tumor angiogenesis have remained elusive. Tumor angiogenesis is coordinated by the activation of both cancer cells and vascular endothelial cells. Whether the YAP signalingpathway can regulate the intercellular interaction between cancer cells and endothelial cellsis essentially unknown.Results: We showed here that conditioned media from YAP overexpressed breast cancer cells (CM-YAP+) could promote angiogenesis, accompanied byincreased tube formation, migration, and proliferation of human umbilical vein endothelial cells (HUVECs). Down regulation of YAP in HUVECs reversed CM-YAP+ induced angiogenesis.CM-YAP+ time-dependently activated YAP inHUVECs by dephosphorylating YAP and increasing nuclear translocation.We also identified that both G13-RhoA and PI3K/Akt signaling pathway were necessary for CM-YAP+ induced activation of YAP.Besides, connective tissue growth factor (CTGF) and angiopoietin-2 (ANG-2)actedas down-stream of YAP in HUVECs to promote angiogenesis.In addition, subcutaneous tumors nude mice model demonstrated that tumors overexpressed YAP revealed moreneovascularization in vivo.Conclusions: YAP-YAP interaction between breastcancer cells and endothelial cellscould promote tumor angiogenesis, supporting that YAP is a potential marker and target fordeveloping novel therapeutic strategies against breast cancer.

Elastase Activity Enhances the Adhesion of Neutrophil and Cancer Cells to Vascular Endothelial Cells

2000 ◽  
Vol 94 (2) ◽  
pp. 153-158 ◽  
Author(s):  
Fumiaki Nozawa ◽  
Masahiko Hirota ◽  
Akihiro Okabe ◽  
Muneyuki Shibata ◽  
Takeshi Iwamura ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cancer Cells ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Elastase Activity
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