A copper-mediated on–off–on gold nanocluster for endogenous GSH sensing to drive cancer cell recognition

2019 ◽  
Vol 7 (13) ◽  
pp. 2169-2176 ◽  
Author(s):  
Hemiao Zhao ◽  
Xiangping Wen ◽  
Wenyan Li ◽  
Yingqi Li ◽  
Caixia Yin
Keyword(s):  
Tumor Cells ◽  
Cancer Cell ◽  
Cancer Diagnosis ◽  
Potential Application ◽  
Selective Detection ◽  
Cell Recognition ◽  
Gold Nanocluster ◽  
Normal Cells ◽  
Great Potential Application

The AuNCs@Tf-Cu2+system for the sensitive and selective detection of endogenous glutathione (GSH) can illuminate tumor cells rather than normal cells, which implied its great potential application in cancer diagnosis.

A near-infrared biothiol-specific fluorescent probe for cancer cell recognition

The Analyst ◽  
2019 ◽  
Vol 144 (16) ◽  
pp. 4750-4756 ◽  
Author(s):  
Li Liu ◽  
Rui-Jie Lv ◽  
Jong-Kai Leung ◽  
Qian Zou ◽  
Yue Wang ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Fluorescent Probe ◽  
Cancer Cell ◽  
Cancer Diagnosis ◽  
Near Infrared ◽  
Great Promise ◽  
Cell Recognition ◽  
Normal Cells

A novel near-infrared biothiol-specific fluorescent probe can discriminate cancer cells from normal cells showing great promise for cancer diagnosis.

Krebszellkinetik und Krebs-Mehrschritt-Therapie / Cancer Cell Kinetics and Cancer Multistep Therapy

1972 ◽  
Vol 27 (12) ◽  
pp. 1547-1566 ◽  
Author(s):  
Manfred Von Ardenne
Keyword(s):  
Cell Cycle ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Cancer Cell ◽  
Glucose Concentration ◽  
Time Span ◽  
Normal Cells ◽  
Tumor Tissues ◽  
Wide Range ◽  
Sensitive Phase

Basic to the proposed therapeutic usage of the difference in the in-vivo proliferation control between cancer and normal cells are the temporary selective increase in the proliferation rate and number of cancer cells in all kinds of tumors but without increase of the proliferative activity of normal cells. To further this aim, measurements of cellular kinetics are used, in connection with the glycolysis of different tumor tissues under saturation conditions, with the relationship between cancer cell cycle and glycolytic rate, or the local glucose level respectively, with the wide range of glucose concentrations in tumor regions which differ the conditions of supply, with the pO2-value critical for tumor growth (≈ 0.4 Torr), with the pO2-distribution in tumor tissues and the time distribution of cell cycles in human and animal cancerous tissues. From an approximative description of the cytostatic effects in different tumor regions and its validity limits it is estimated that the sensitivity towarts therapy is decreased to as low as one-tenth in poorly supplied tumor regions. These particular fractions of the tumor tissues determine the degree of tumor resistence. Additionally, from these considerations steps can be derived which could be important for multiplying the effect of the cytostatic attack on the critical tumor regions with poor supply conditions. These steps include: a) usage of combinations of cytostatic agents directed against all three sensitive phases of the cell cycle (S-G2-M); b) increase in blood glucose concentration to about 300 mg% for an optimum time span prior to the initiation of the main therapeutic process; c) increase in pO2 of the inspiration air to 320 or 400 Torr and in the degree of pO2 utilization by the use of specific pharmaceutic agents for the chosen time span preceding the main therapy; d) stimulation of tumor vascularization preceding the main therapy; e) decrease in the fraction of tumor cells utilizing glucose and O2 as a consequence of a post-therapy treatment 72 hours after the main therapy. The increase in the fraction of cells in a sensitive phase of the cell cycle is reached folowing synchronization after increasing the glucose concentration until saturation of the glycolytic capacity. Reasons are given, why the cytostatic attack has to be supplemented by other selective mechanisms which damage the tumor cell independent of the phase of the cell cycle. Such a mechanism is the lysosomal cytolytic chain reaction. Here, the death of tumor cells occurring during a sensitive phase of the cell cycle as a consequence of the cytostatic attack helps to damage cancer cells which are in the insensitive phase. A further mechanism of this kind is the immunological attack, which is also a component of multi-step cancer therapy

3D morphometric analysis to yield high sensitivity and specificity enumeration of circulating tumor cells.

2013 ◽  
Vol 31 (15_suppl) ◽  
pp. e22031-e22031
Author(s):  
Michael Meyer ◽  
Thomas Neumann ◽  
Rahul Katdare ◽  
Chris Presley ◽  
Jon Hayenga ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Circulating Tumor Cells ◽  
Cancer Cell ◽  
Blood Cells ◽  
Breast Cancer Cells ◽  
Cell Detection ◽  
Normal Cells ◽  
Adaptive Boosting

e22031 Background: The enumeration of circulating tumor cells (CTCs) has become a common method to assess cancer treatment efficacy. In this study, we propose to test our ability to detect and enumerate CTCs using a morphometric classifier based on 3D cell features to distinguish normal cells from lysed blood and breast cancer cells. Methods: Commercially available normal whole blood was lysed to destroy red blood cells, leaving white blood cells and some cell debris. These cells and breast cancer cells from the SK-BR-3 cell line were studied. The cells were stained with hematoxylin, then were automatically imaged using VisionGate’s 3D cell imaging system (Cell-CT) that unambiguously renders individual cells with isometric, sub-micron resolution. Image libraries of cells were created. For each cell, 683 morphology features were computed. Features characterize various aspects of the cell such as chromatin distribution in the nucleus, nuclear volume and shape and nuclear to cell volume ratios. The true cell diagnosis for each cell was determined by a cytotechnologist and added to the feature set. Cross-validated classifiers were created using the technique of adaptive boosting that combines a sub-set of the features into a single score that best correlated with the binary cell diagnoses. Results: 3,256 normal cells or other normal objects and 1,843 breast cancer cells were studied. A classifier that distinguished normal cells from cancer cells was created that used the strongest 25 3D morphology features. The morphometric classifier had an area under the ROC curve that measured 0.9998. This classifier could be operated with near perfect specificity and a cancer cell sensitivity of 95%. Conclusions: Performance of automated, 3D morphometric classifiers for cancer cell detection suggests highly accurate CTC enumeration with implications for patient management and prediction of cancer progression.

scholarly journals Spider Toxin Peptide-Induced NIR Gold Nanocluster Fabrication for GSH-Responsive Cancer Cell Imaging and Nuclei Translocation

2021 ◽  
Vol 9 ◽  
Author(s):  
Huaxin Tan ◽  
Sisi Liu ◽  
Yaolin He ◽  
Guofeng Cheng ◽  
Yu Zhang ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Near Infrared ◽  
Nuclear Targeting ◽  
Gold Nanocluster ◽  
Cancerous Cell ◽  
Nir Fluorescence ◽  
High Level ◽  
Induced Aggregation

Goldnanoclusters (GNCs) have become a promising nanomaterial for bioimaging because of their unique optical properties and biocompatibility. In this study, lycosin-I peptide, which possesses a highly selective anticancer activity by affecting the permeability of cancer cell membrane, was firstly modified for constructing fluorescent GNCs (LGNCs) for bioimaging of tumor cells. The obtained LGNCs exhibited strong near-infrared (NIR) fluorescence, which can be further enhanced by the peptide-induced aggregation and selectively stained three cancerous cell lines over normal cell lines with low intrinsic toxicity. After uptake by tumor cells, LGNC aggregates can be depolymerized into ultrasmall nanoclusters by high-level glutathione (GSH) and realize the nuclear targeting translocation. Collectively, our work suggests the potential of natural active biomolecules in designing NIR fluorescent GNCs for bioimaging.

Epigenetic Modifiers and Their Potential Application in Colorectal Cancer Diagnosis and Therapy

2020 ◽  
Vol 25 (2) ◽  
pp. 95-109
Author(s):  
Sapnita Shinde ◽  
Saurabh Saxena ◽  
Vineeta Dixit ◽  
Atul K. Tiwari ◽  
Naveen K. Vishvakarma ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Diagnosis ◽  
Potential Application ◽  
Diagnosis And Therapy ◽  
Epigenetic Modifiers ◽  
Cancer Diagnosis And Therapy

The Role of Reactive Oxygen Species in Tumor Treatment and its Impact on Bone Marrow Hematopoiesis

2020 ◽  
Vol 21 (5) ◽  
pp. 477-498
Author(s):  
Yongfeng Chen ◽  
Xingjing Luo ◽  
Zhenyou Zou ◽  
Yong Liang
Keyword(s):  
Reactive Oxygen Species ◽  
Bone Marrow ◽  
Oxidative Damage ◽  
Tumor Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Tumor Treatment ◽  
Normal Cells ◽  
Treatment And Prevention

Reactive oxygen species (ROS), an important molecule inducing oxidative stress in organisms, play a key role in tumorigenesis, tumor progression and recurrence. Recent findings on ROS have shown that ROS can be used to treat cancer as they accelerate the death of tumor cells. At present, pro-oxidant drugs that are intended to increase ROS levels of the tumor cells have been widely used in the clinic. However, ROS are a double-edged sword in the treatment of tumors. High levels of ROS induce not only the death of tumor cells but also oxidative damage to normal cells, especially bone marrow hemopoietic cells, which leads to bone marrow suppression and (or) other side effects, weak efficacy of tumor treatment and even threatening patients’ life. How to enhance the killing effect of ROS on tumor cells while avoiding oxidative damage to the normal cells has become an urgent issue. This study is a review of the latest progress in the role of ROS-mediated programmed death in tumor treatment and prevention and treatment of oxidative damage in bone marrow induced by ROS.

scholarly journals Hypoxia-Induced Cancer Cell Responses Driving Radioresistance of Hypoxic Tumors: Approaches to Targeting and Radiosensitizing

Cancers ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1102
Author(s):  
Alexander E. Kabakov ◽  
Anna O. Yakimova
Keyword(s):  
Heat Shock ◽  
Tumor Cells ◽  
Cancer Cell ◽  
Epithelial Mesenchymal Transition ◽  
Liver Tumors ◽  
Oxygen Deficiency ◽  
Transarterial Embolization ◽  
Antiangiogenic Therapy ◽  
Adaptation To Hypoxia ◽  
Mesenchymal Transition

Within aggressive malignancies, there usually are the “hypoxic zones”—poorly vascularized regions where tumor cells undergo oxygen deficiency through inadequate blood supply. Besides, hypoxia may arise in tumors as a result of antiangiogenic therapy or transarterial embolization. Adapting to hypoxia, tumor cells acquire a hypoxia-resistant phenotype with the characteristic alterations in signaling, gene expression and metabolism. Both the lack of oxygen by itself and the hypoxia-responsive phenotypic modulations render tumor cells more radioresistant, so that hypoxic tumors are a serious challenge for radiotherapy. An understanding of causes of the radioresistance of hypoxic tumors would help to develop novel ways for overcoming this challenge. Molecular targets for and various approaches to radiosensitizing hypoxic tumors are considered in the present review. It is here analyzed how the hypoxia-induced cellular responses involving hypoxia-inducible factor-1, heat shock transcription factor 1, heat shock proteins, glucose-regulated proteins, epigenetic regulators, autophagy, energy metabolism reprogramming, epithelial–mesenchymal transition and exosome generation contribute to the radioresistance of hypoxic tumors or may be inhibited for attenuating this radioresistance. The pretreatments with a multitarget inhibition of the cancer cell adaptation to hypoxia seem to be a promising approach to sensitizing hypoxic carcinomas, gliomas, lymphomas, sarcomas to radiotherapy and, also, liver tumors to radioembolization.

scholarly journals Productive Infection of Human Breast Cancer Cell Lines with Human Cytomegalovirus (HCMV)

Pathogens ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 641
Author(s):  
Kaitlin M. Branch ◽  
Erica C. Garcia ◽  
Yin Maggie Chen ◽  
Matthew McGregor ◽  
Mikayla Min ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Tumor ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines ◽  
Human Breast ◽  
Breast Tumor Cells

Breast cancer is the leading cause of cancer deaths among women worldwide. There are many known risk factors for breast cancer, but the role of infectious disease remains unclear. Human cytomegalovirus (HCMV) is a widespread herpesvirus that usually causes little disease. Because HCMV has been detected in breast tumor biopsy samples and is frequently transmitted via human breast milk, we investigated HCMV replication in breast tumor cells. Four human breast cancer cell lines with different expression profiles for the key diagnostic markers of the estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2), were infected with a bacterial artificial chromosome-derived HCMV clinical strain TB40/E tagged with green fluorescent protein (GFP). Fluorescence microscopy confirmed that all four breast cancer cell lines supported virus entry. RNA was isolated from infected cells and the expression of immediate early (UL123), early (UL54), and late (UL111A) genes was confirmed using PCR. Viral proteins were detected by immunoblotting, and viral progeny were produced during the infection of breast tumor cells, as evidenced by subsequent infection of fibroblasts with culture supernatants. These results demonstrate that breast tumor cells support productive HCMV infection and could indicate that HCMV replication may play a role in breast cancer progression.

scholarly journals Design, Synthesis, Molecular Modeling and Antitumor Evaluation of Novel Indolyl-Pyrimidine Derivatives with EGFR Inhibitory Activity

Molecules ◽  
2021 ◽  
Vol 26 (7) ◽  
pp. 1838
Author(s):  
Naglaa M. Ahmed ◽  
Mahmoud M. Youns ◽  
Moustafa K. Soltan ◽  
Ahmed M. Said
Keyword(s):  
Molecular Modeling ◽  
Antitumor Activity ◽  
Cell Lines ◽  
Cancer Cell ◽  
Antiproliferative Activity ◽  
Antitumor Agents ◽  
Cancer Cell Lines ◽  
Normal Cells

Scaffolds hybridization is a well-known drug design strategy for antitumor agents. Herein, series of novel indolyl-pyrimidine hybrids were synthesized and evaluated in vitro and in vivo for their antitumor activity. The in vitro antiproliferative activity of all compounds was obtained against MCF-7, HepG2, and HCT-116 cancer cell lines, as well as against WI38 normal cells using the resazurin assay. Compounds 1–4 showed broad spectrum cytotoxic activity against all these cancer cell lines compared to normal cells. Compound 4g showed potent antiproliferative activity against these cell lines (IC50 = 5.1, 5.02, and 6.6 μM, respectively) comparable to the standard treatment (5-FU and erlotinib). In addition, the most promising group of compounds was further evaluated for their in vivo antitumor efficacy against EAC tumor bearing mice. Notably, compound 4g showed the most potent in vivo antitumor activity. The most active compounds were evaluated for their EGFR inhibitory (range 53–79 %) activity. Compound 4g was found to be the most active compound against EGFR (IC50 = 0.25 µM) showing equipotency as the reference treatment (erlotinib). Molecular modeling study was performed on compound 4g revealed a proper binding of this compound inside the EGFR active site comparable to erlotinib. The data suggest that compound 4g could be used as a potential anticancer agent.

Cytokine and inflammatory mediators are associated with cytotoxic, anti-inflammatory and apoptotic activity of honeybee venom

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Mohamed A. Salama ◽  
Mohamed A. Younis ◽  
Roba M. Talaat
Keyword(s):  
Nitric Oxide ◽  
Cell Lines ◽  
Cancer Cell ◽  
Hela Cells ◽  
No Production ◽  
Hep G2 ◽  
Normal Cells ◽  
Tnf Α ◽  
Ifn Γ ◽  
Mcf 7

AbstractObjectiveThe present study aimed to evaluate cytotoxic, apoptotic, and anti-inflammatory properties of bee venom (BV) as well as changes in cytokine secretion levels and nitric oxide (NO) production using three different cancer cell lines [liver (Hep-G2), breast (MCF-7), and cervical (HPV-18 infected HeLa cells)] and two normal cells (splenocytes and macrophages (MQ).MethodsCytotoxic activity of BV against tumor cell lines and normal splenocytes/MQ was tested by MTT assay. By ELISA (ELISA); Tumor necrosis factor (TNF-α), Interleukine (IL-10) and interferon (IFN-γ) were measured. Caspase three expressions was evaluated using reverse transcription-polymerase chain reaction (RT-PCR). Nitric oxide (NO) was estimated using a colorimetric assay.ResultsBV has a significant cytotoxic effect on all cell lines in a dose- and time-dependent manner; none of them was toxic for normal cells. Treating Hep-G2 cells with BV showed a reduction in IL-10, elevation in TNF-α with no change in IFN-γ level. MCF-7 cells have low IL-10 and TNF-α and high IFN-γ production level. Elevation of IL-10 and IFN-γ coincides with a reduction in TNF-α level was demonstrated in HeLa cells. The expression of Caspase three was dramatically increased with elevation in BV concentration in all tested cancer cell lines. A gradual decrease in NO production by MQ with increasing BV dose was observed.ConclusionTaken together, our results stressed on the importance of BV as a potent anti-tumor agent against various types of cancers (Liver, Breast, and Cervix). Further steps towards the use of BV for pharmacological purposes must be done.

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