Visualization of radiation-induced cell cycle-associated events in tumor cells expressing the fusion protein of Azami Green and the destruction box of human Geminin

2009 ◽  
Vol 389 (3) ◽  
pp. 426-430 ◽  
Author(s):  
Mayuko Ishikawa ◽  
Yusuke Ogihara ◽  
Masahiko Miura
Keyword(s):  
Cell Cycle ◽  
Fusion Protein ◽  
Tumor Cells ◽  
Radiation Induced ◽  
Destruction Box

scholarly journals Zinc Oxide Nanoparticles Can Intervene in Radiation-Induced Senescence and Eradicate Residual Tumor Cells

Cancers ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 2989
Author(s):  
Nadine Wiesmann ◽  
Rita Gieringer ◽  
Melanie Viel ◽  
Jonas Eckrich ◽  
Wolfgang Tremel ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Zinc Oxide ◽  
Tumor Cells ◽  
Zinc Oxide Nanoparticles ◽  
Tumor Therapy ◽  
Cell Mass ◽  
The Body ◽  
Oxide Nanoparticles ◽  
Zno Nps ◽  
Radiation Induced

Despite recent advancements in tumor therapy, metastasis and tumor relapse remain major complications hindering the complete recovery of many cancer patients. Dormant tumor cells, which reside in the body, possess the ability to re-enter the cell cycle after therapy. This phenomenon has been attributed to therapy-induced senescence. We show that these cells could be targeted by the use of zinc oxide nanoparticles (ZnO NPs). In the present study, the properties of tumor cells after survival of 16 Gy gamma-irradiation were investigated in detail. Analysis of morphological features, proliferation, cell cycle distribution, and protein expression revealed classical hallmarks of senescent cells among the remnant cell mass after irradiation. The observed radiation-induced senescence was associated with the increased ability to withstand further irradiation. Additionally, tumor cells were able to re-enter the cell cycle and proliferate again after weeks. Treatment with ZnO NPs was evaluated as a therapeutical approach to target senescent cells. ZnO NPs were suitable to induce cell death in senescent, irradiation-resistant tumor cells. Our findings underline the pathophysiological relevance of remnant tumor cells that survived first-line radiotherapy. Additionally, we highlight the therapeutic potential of ZnO NPs for targeting senescent tumor cells.

The assessment of prokaryotic addictive modules’ activity in the context of seeking novel immunotoxins

2017 ◽  
Vol 5 ◽  
pp. 59-63
Author(s):  
Katarzyna Oszajca ◽  
Łukasz Wieteska ◽  
Magdalena Cybula ◽  
Janusz Szemraj
Keyword(s):  
Cell Cycle ◽  
Targeted Therapy ◽  
Fusion Protein ◽  
Cell Cycle Arrest ◽  
Tumor Cells ◽  
Cell Lines ◽  
Cycle Arrest ◽  
Potential Component ◽  
New Type ◽  
Therapy Strategies

Despite of the fact that current anticancer chemotherapeutics have many beneficial achievements, there is an urgent need for new efficient therapies. A new type of drugs which are extensively investigated are immunotoxinshybrid proteins that consist of cytotoxic component and second part which is responsible for selective binding to the receptors on tumor cells. Unfortunately, this group of therapeutics still has many drawbacks. There is a strong demand for research on a new substances and develo-ping targeted therapy strategies. In the present study we tested VapC toxin derived from prokaryotic addictive modules as a potential component in the construction of immunotoxins. Investigated fusion protein consists of VapC toxin has RNase activity and digests total RNA in various treatment times. Moreover, studied protein displays proapoptotic properties and cell cycle arrest in selected cancer cell lines.

scholarly journals Radiobiological effects of the alpha emitter Ra-223 on tumor cells

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Kristina Bannik ◽  
Balázs Madas ◽  
Marco Jarzombek ◽  
Andreas Sutter ◽  
Gerhard Siemeister ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Tumor Cells ◽  
Biological Effects ◽  
Tumor Cell Lines ◽  
Radiation Induced ◽  
Radiobiological Effects ◽  
Dose Dependent ◽  
Α Particles

AbstractTargeted alpha therapy is an emerging innovative approach for the treatment of advanced cancers, in which targeting agents deliver radionuclides directly to tumors and metastases. The biological effects of α-radiation are still not fully understood - partly due to the lack of sufficiently accurate research methods. The range of α-particles is <100 μm, and therefore, standard in vitro assays may underestimate α-radiation-specific radiation effects. In this report we focus on α-radiation-induced DNA lesions, DNA repair as well as cellular responses to DNA damage. Herein, we used Ra-223 to deliver α-particles to various tumor cells in a Transwell system. We evaluated the time and dose-dependent biological effects of α-radiation on several tumor cell lines by biological endpoints such as clonogenic survival, cell cycle distribution, comet assay, foci analysis for DNA damage, and calculated the absorbed dose by Monte-Carlo simulations. The radiobiological effects of Ra-223 in various tumor cell lines were evaluated using a novel in vitro assay designed to assess α-radiation-mediated effects. The α-radiation induced increasing levels of DNA double-strand breaks (DSBs) as detected by the formation of 53BP1 foci in a time- and dose-dependent manner in tumor cells. Short-term exposure (1–8 h) of different tumor cells to α-radiation was sufficient to double the number of cells in G2/M phase, reduced cell survival to 11–20% and also increased DNA fragmentation measured by tail intensity (from 1.4 to 3.9) dose-dependently. The α-particle component of Ra-223 radiation caused most of the Ra-223 radiation-induced biological effects such as DNA DSBs, cell cycle arrest and micronuclei formation, leading ultimately to cell death. The variable effects of α-radiation onto the different tumor cells demonstrated that tumor cells show diverse sensitivity towards damage caused by α-radiation. If these differences are caused by genetic alterations and if the sensitivity could be modulated by the use of DNA damage repair inhibitors remains a wide field for further investigations.

TRAIL targets cell cycle arrested tumor cells

2012 ◽  
Vol 224 (03) ◽  
Author(s):  
F Wachter ◽  
M Grunert ◽  
I Jeremias ◽  
H Ehrhardt
Keyword(s):  
Cell Cycle ◽  
Tumor Cells

Antitumor Activity and Underlying Mechanism of Phomoxanthone B in MCF7 Cells

2020 ◽  
Vol 20 ◽  
Author(s):  
Chuan Chen ◽  
Ziyue Zhao ◽  
Qian Dong ◽  
XueHui Gao ◽  
Huibin Xu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Antitumor Activity ◽  
Oxidative Phosphorylation ◽  
Tumor Cells ◽  
Transcriptome Analysis ◽  
Mcf7 Cells ◽  
Er Positive ◽  
Induced Apoptosis ◽  
Positive Breast Cancer

Background:: Xanthones are a class of heterocyclic natural products, which are promising sources of anticancer leads. Phomoxanthone B（PXB）and Phomoxanthone A（PXA）are xanthone dimers. PXA is well studied as an anti-cancer agent, but PXB is not. In our study, PXB was isolated from the endophytic fungus Phomopsis sp. By254. Objective:: The purpose of this study was to identify the underlying anti-tumor mechanisms of PXB in breast cancer MCF7 cell line. Methods:: Apoptosis, cell cycle, proliferation, invasion and migration assays were used to assess the antitumor activity of PXB. RNA sequencing was used to analyze the effect of PXB treatment on gene expression in MCF7 cells. Results:: PXB showed cytotoxicity toward a variety of tumor cells, especially MCF7 cells. PXB inhibited the migration and invasion, arrested cell cycle at G2/M phase and induced apoptosis associated with caspase-3 activation in MCF7 cells. The detailed transcriptome analysis revealed that PXB affected several pathways related to tumorigenesis, metabolisms-, and oxidative phosphorylation in MCF7 cells. KEGG transcriptome analysis revealed that PXB upregulated pro-survival signal pathways such as MAPK, PI3K-AKT and STAT3 pathways. We found that PXB also significantly upregulated the expression of IL24, DDIT3 and XAF1, which may contribute to PXB-induced apoptosis. We further found that PXB may downregulate oxidative phosphorylation by decreasing the expression of electron transport chain genes, especially MT-ND1, which is a potential unfavorable prognostic marker for ER-positive breast cancer. Conclusion:: PXB exerts strong cytotoxicity against human tumor cells and has a potential for ER-positive breast cancer treatment.

Tumor cells suppress radiation-induced immunity by hijacking caspase 9 signaling

2020 ◽  
Vol 21 (5) ◽  
pp. 546-554 ◽  
Author(s):  
Chuanhui Han ◽  
Zhida Liu ◽  
Yunjia Zhang ◽  
Aijun Shen ◽  
Chunbo Dong ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Caspase 9 ◽  
Radiation Induced ◽  
Induced Immunity

scholarly journals Bi-Functional Radiotheranostics of 188Re-Liposome-Fcy-hEGF for Radio- and Chemo-Therapy of EGFR-Overexpressing Cancer Cells

2021 ◽  
Vol 22 (4) ◽  
pp. 1902 ◽  
Author(s):  
Yi-Shu Huang ◽  
Wei-Chuan Hsu ◽  
Chien-Hong Lin ◽  
Sheng-Nan Lo ◽  
Chu-Nian Cheng ◽  
...  
Keyword(s):  
Fusion Protein ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Cytotoxic Effect ◽  
Cytosine Deaminase ◽  
Growth Factor Receptor ◽  
Size Exclusion ◽  
Specific Therapy ◽  
Egfr Expression ◽  
Epidermal Growth

Epidermal growth factor receptor (EGFR) specific therapeutics is of great importance in cancer treatment. Fcy-hEGF fusion protein, composed of yeast cytosine deaminase (Fcy) and human EGF (hEGF), is capable of binding to EGFR and enzymatically convert 5-fluorocytosine (5-FC) to 1000-fold toxic 5-fluorocuracil (5-FU), thereby inhibiting the growth of EGFR-expressing tumor cells. To develop EGFR-specific therapy, 188Re-liposome-Fcy-hEGF was constructed by insertion of Fcy-hEGF fusion protein onto the surface of liposomes encapsulating of 188Re. Western blotting, MALDI-TOF, column size exclusion and flow cytometry were used to confirm the conjugation and bio-activity of 188Re-liposome-Fcy-hEGF. Cell lines with EGFR expression were subjected to treat with 188Re-liposome-Fcy-hEGF/5-FC in the presence of 5-FC. The 188Re-liposome-Fcy-hEGF/5-FC revealed a better cytotoxic effect for cancer cells than the treatment of liposome-Fcy-hEGF/5-FC or 188Re-liposome-Fcy-hEGF alone. The therapeutics has radio- and chemo-toxicity simultaneously and specifically target to EGFR-expression tumor cells, thereby achieving synergistic anticancer activity.

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