Combinatorial discovery of Mo-based polyoxometalate clusters for tumor photothermal therapy and normal cell protection

2020 ◽  
Vol 8 (21) ◽  
pp. 6017-6024
Author(s):  
Wancheng Zhao ◽  
Jingguo Wang ◽  
Henan Wang ◽  
Shuting Lu ◽  
Yan Song ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Photothermal Therapy ◽  
Normal Cell ◽  
Cell Protection ◽  
Normal Cells

Molybdenum (Mo)-based polyoxometalate clusters can kill cancer cells selectively by PTT assay and protect the normal cells by scavenging ROS effectively.

Multifunctional polyphosphazene-coated multi-walled carbon nanotubes for the synergistic treatment of redox-responsive chemotherapy and effective photothermal therapy

2017 ◽  
Vol 8 (45) ◽  
pp. 6938-6942 ◽  
Author(s):  
Daquan Wang ◽  
Yibo Ren ◽  
Yongping Shao ◽  
Lingjie Meng
Keyword(s):  
Carbon Nanotubes ◽  
Drug Delivery ◽  
Cancer Cells ◽  
Drug Delivery System ◽  
Anticancer Drug ◽  
Photothermal Therapy ◽  
Normal Cells ◽  
Redox Responsive ◽  
Multi Walled Carbon Nanotubes ◽  
Walled Carbon Nanotubes

A multifunctional drug delivery system for chemo-photothermal therapeutics was developed by coating an anticancer-drug-containing polyphosphazene onto multi-walled carbon nanotubes, which could selectively suppress and kill cancer cells, but negligibly affect normal cells.

scholarly journals The Ultimate Substance to Cause Cancer Is a Hydrogen Ion and Cancer Cells Stop its Division-Multiplication and Return to Normal Cells by Supplying Oxygen as Hydrogen Acceptor, from Theoretical Research

2021 ◽  
Author(s):  
Nobuo Tomizawa
Keyword(s):  
Theoretical Model ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Normal Cell ◽  
Medical Science ◽  
Theoretical Models ◽  
Theoretical Work ◽  
Theoretical Research ◽  
Hydrogen Ions ◽  
Normal Cells

(1)A fundamental viewpoint about cancer cellsAt the present time, methods of treatment for cancer base on the viewpoint that cancer cells make humans deaths, therefore a treatment destroys and kills cancer cells and saves patients. But this conception strikes against the limit on treatment. A cancer cell changed from a normal cell of a human, it does not invade from outside and harm a human like virus. A cancer cell is derived from a human cell, therefore when we aim to destroy cancer cells, this attack damages to other normal cells and weaken vital energy of a human. Here there is the limit of treatment for cancer.In opposition to these thoughts, this theory is based on the viewpoint that normal cells faced to critical situation to live and changed its system to survive under the situation and that are certainly cancer cells. The reason why a cancer cell has tough vitality to make a human death is the result to acquire the ability for existing under such a situation. Therefore a treatment for cancer is not to destroy and to kill but to remove factors that prevent normal cells from living orderly. Then cancer cells become unnecessary to derive a tough vitality. And its rapid division and multiplication will stop and return to normal cells.I built the theoretical model as follows. A cell becomes lack of oxygen that is necessary to live. Then hydrogen ions emerge in that cell. Hydrogen ions promote division and multiplication. Take these hydrogen ions out by supplying oxygen like a normal cell doing, and cancer cells will stop division and return to normal cells.This research intends to explain by facts already known and prove this model on,how hydrogen ions emerge in cells?how hydrogen ions promote cell division? Thenhow a treatment for cancer is possible?(2)The division of works of building theoretical models and experiments on biology and medical scienceSome historical discoveries on physics have walked on the process that a theoretical research predicts the existence of materials or the law and some experiments prove it. Physics is divided into two areas. One is theoretical physics that builds theoretical models and another is experimental physics that proves those models by experiments. In medical science and biology, usually one researcher builds a supposition and proves it by experiments. Theoretical work and verification by experimental work are not divided. A theoretical model without experimental proof is not enough recognized its medical or biological value.However more multiple researches will be possible by dividing theoretical work to build theoretical models and experimental work to verify it in the field of cancer that is not solved an ultimate cause and a mechanism to change from normal cells. And it should value theoretical researches that are not yet verified by experiments.This treatise is the theoretical model that is not proved by experiments. I illustrated specific ways for experiments to prove in Chapter 4, “The principle and practical methods of medical treatment for cancer of human beings, (1)Supply oxygen to cultured cancer cells, and multiplication of cancer cells will stop”.I hope that scientists of medical science and biology would prove it by experiments.

scholarly journals Benzimidazole based Pt(ii) complexes with better normal cell viability than cisplatin: synthesis, substitution behavior, cytotoxicity, DNA binding and DFT study

RSC Advances ◽  
2016 ◽  
Vol 6 (80) ◽  
pp. 76600-76613 ◽  
Author(s):  
Ishani Mitra ◽  
Subhajit Mukherjee ◽  
Venkata P. Reddy B. ◽  
Subrata Dasgupta ◽  
Jagadeesh C. Bose K ◽  
...  
Keyword(s):  
Dna Binding ◽  
Cell Viability ◽  
Cancer Cells ◽  
Normal Cell ◽  
Water Soluble ◽  
Dft Study ◽  
Normal Cells

Water soluble Pt(ii) complexes with higher viability towards normal cells and comparable cytotoxicity to cancer cells as compared to cisplatin.

scholarly journals The Effect of Diopatra claparedii Grube, 1878 Aqueous Extract on Chang Liver and Human Primary Glioblastoma (U-87) Cell Lines

2019 ◽  
Vol 1 (3) ◽  
pp. 56-67
Author(s):  
Amirah Idris ◽  
Izwandy Idris ◽  
Wan Iryani Wan Ismail
Keyword(s):  
Cell Growth ◽  
Cancer Cells ◽  
Cell Lines ◽  
Aqueous Extract ◽  
Normal Cell ◽  
Cellular Growth ◽  
Growth Effect ◽  
Normal Cells ◽  
Primary Glioblastoma ◽  
Chang Liver

Due to the distinctive regenerative ability of Diopatra claparedii Grube, 1878, the local marine polychaete has the potential as a cellular growth agent. In this study, the growth effect was investigated in normal cells and cancer cells. Different concentrations (0-100mg/mL) of D. claparedii aqueous extract were tested on Chang Liver (normal cells), and Human Primary Glioblastoma (U-87) (cancer cells) cell lines for 24, 48 and 72 hours. Percentage of cell viability was evaluated by [2-(4, 5-dimethyl-2-thiazolyl)-3, 5-diphenyl-2H tetrazolium bromide] (MTT) assay. The findings suggested that the extract had a proliferative effect on normal cell growth when tested at lower doses (<60 mg/mL) but inhibited normal cells at concentrations >80 mg/mL in all incubation periods. Meanwhile, it showed the cytotoxic effect on cancer cells only after 48h when treated with all concentrations. As demonstrated, the extract could induce normal cell growth without causing abnormal or cancer cells progression at low concentrations after 48h and 72h.

scholarly journals Melatonin in Mitochondria: Mitigating Clear and Present Dangers

Physiology ◽  
2020 ◽  
Vol 35 (2) ◽  
pp. 86-95 ◽  
Author(s):  
Russel J. Reiter ◽  
Qiang Ma ◽  
Ramaswamy Sharma
Keyword(s):  
Glucose Metabolism ◽  
Cancer Cells ◽  
Normal Cell ◽  
Cell Phenotype ◽  
Acetyl Coa ◽  
Normal Cells ◽  
Melatonin Synthesis ◽  
Rate Limiting ◽  
Melatonin Production

In cancer cells, glucose is primarily metabolized to pyruvate and then to lactate in the cytosol. By allowing the conversion of pyruvate to acetyl-CoA in mitochondria, melatonin reprograms glucose metabolism in cancer cells to a normal cell phenotype. Acetyl-CoA in the mitochondria also serves as a necessary co-factor for the rate-limiting enzyme in melatonin synthesis, thus ensuring melatonin production in mitochondria of normal cells.

Molecular Studies on Novel Antitumor Bis 1,4-Dihydropyridine Derivatives Against Lung Carcinoma and their Limited Side Effects on Normal Melanocytes

2019 ◽  
Vol 18 (15) ◽  
pp. 2156-2168 ◽  
Author(s):  
Magda F. Mohamed ◽  
Nada S. Ibrahim ◽  
Ahmed H.M. Elwahy ◽  
Ismail A. Abdelhamid
Keyword(s):  
Breast Cancer ◽  
Side Effects ◽  
Cancer Cells ◽  
Cell Line ◽  
Lung Carcinoma ◽  
Carcinoma Cell ◽  
Normal Cells ◽  
Lung Carcinoma Cell Line ◽  
Molecular Studies ◽  
Dihydropyridine Derivatives

Background: Cancer is a complex genetic disease which is characterized by an abnormal cell growth, invasion and spreading to other parts of the body. There are several factors that lead to cancer by causing DNA damage and the impairment of its repair. Treatment of cancer using the chemotherapeutic drugs have adverse side effects such as toxicity as they lose their specificity toward cancer cells and affect also normal cells. Moreover, the cancer cells can resist the chemotherapeutic agents and make them ineffective. For these reasons, much attentions have been paid to develop new drugs with limited side effects on normal cells and to diminish cancer resistance to drug chemotherapy. Recently, some 1,4-dihydropyridine derivatives were reported to act as Multi-Drug Resistance (MDR) modulators that inhibit p-glycoprotein which is responsible for the inability of drugs to enter the cancer cells. Also 1,4-DHPs have antimutagenic properties against chemicals via modulating DNA repair when studied on drosophila. Objective: The objective of this study is the synthesis of bis 1,4-DHPs incorporating ester as well as ether linkages and evaluate the anticancer activity of new compounds for synergistic purpose. Different genetic tools were used in an attempt to know the mechanism of action of this compound against lung cancer. Method: An efficient one pot synthesis of bis 1,4-DHPs using 3-aminocrotononitrile and bis(aldehydes) has been developed. The cytotoxic effect against human cell lines MCF7, and A549 cell lines was evaluated. Results: All compounds exhibited better cytotoxicity toward lung carcinoma cells than breast cancer cells. With respect to lung carcinoma cell line (A549), compound 10 was the most active compound and the three other compounds 7, 8, and 9 showed comparable IC50 values. In case of breast cancer cell line (MCF7), the most active one was compound 7, while compound 8 recorded the least activity. Conclusion: we have developed an efficient method for the synthesis of novel bis 1,4-dihydropyridine derivatives incorporating ester or ether linkage. All compounds showed better cytotoxicity results against A549 than MCF7, so that lung carcinoma cell line was chosen to perform the molecular studies on it. The results showed that all compounds (7, 8, 9 and 10) caused cell cycle arrest at G1 phase. The molecular docking study on CDK2 confirmed the results of cell cycle assay which showed good binding energy between the compounds and the active site of enzyme indicating the inhibition of the enzyme.

Single-chain antibody-decorated Au nanocages@liposomal layer nanoprobes for targeted SERS imaging and remote-controlled photothermal therapy of melanoma cancer cells

2021 ◽  
Vol 124 ◽  
pp. 112086
Author(s):  
Ghazal Farahavar ◽  
Samira Sadat Abolmaali ◽  
Foroogh Nejatollahi ◽  
Amin Safaie ◽  
Sanaz Javanmardi ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Photothermal Therapy ◽  
Single Chain ◽  
Single Chain Antibody ◽  
Melanoma Cancer ◽  
Sers Imaging

scholarly journals Normal cells repel WWOX-negative or -dysfunctional cancer cells via WWOX cell surface epitope 286-299

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Yu-An Chen ◽  
Yong-Da Sie ◽  
Tsung-Yun Liu ◽  
Hsiang-Ling Kuo ◽  
Pei-Yi Chou ◽  
...  
Keyword(s):  
Cell Surface ◽  
Cancer Cells ◽  
Room Temperature ◽  
Metastatic Cancer ◽  
Normal Cells ◽  
Tgfβ Receptor ◽  
Membrane Type ◽  
Cell Invasiveness ◽  
And Control ◽  
Metastatic Cancer Cells

AbstractMetastatic cancer cells are frequently deficient in WWOX protein or express dysfunctional WWOX (designated WWOXd). Here, we determined that functional WWOX-expressing (WWOXf) cells migrate collectively and expel the individually migrating WWOXd cells. For return, WWOXd cells induces apoptosis of WWOXf cells from a remote distance. Survival of WWOXd from the cell-to-cell encounter is due to activation of the survival IκBα/ERK/WWOX signaling. Mechanistically, cell surface epitope WWOX286-299 (repl) in WWOXf repels the invading WWOXd to undergo retrograde migration. However, when epitope WWOX7-21 (gre) is exposed, WWOXf greets WWOXd to migrate forward for merge. WWOX binds membrane type II TGFβ receptor (TβRII), and TβRII IgG-pretreated WWOXf greet WWOXd to migrate forward and merge with each other. In contrast, TβRII IgG-pretreated WWOXd loses recognition by WWOXf, and WWOXf mediates apoptosis of WWOXd. The observatons suggest that normal cells can be activated to attack metastatic cancer cells. WWOXd cells are less efficient in generating Ca2+ influx and undergo non-apoptotic explosion in response to UV irradiation in room temperature. WWOXf cells exhibit bubbling cell death and Ca2+ influx effectively caused by UV or apoptotic stress. Together, membrane WWOX/TβRII complex is needed for cell-to-cell recognition, maintaining the efficacy of Ca2+ influx, and control of cell invasiveness.

scholarly journals Quantum Dots as a Good Carriers of Unsymmetrical Bisacridines for Modulating Cellular Uptake and the Biological Response in Lung and Colon Cancer Cells

Nanomaterials ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 462 ◽  
Author(s):  
Joanna Pilch ◽  
Patrycja Kowalik ◽  
Piotr Bujak ◽  
Anna M. Nowicka ◽  
Ewa Augustin
Keyword(s):  
Quantum Dots ◽  
Cancer Cells ◽  
Cellular Uptake ◽  
Laser Scanning ◽  
Biological Response ◽  
Drug Carriers ◽  
Confocal Laser ◽  
Normal Cells ◽  
H460 Cells ◽  
Hct116 Cells

Nanotechnology-based drug delivery provides a promising area for improving the efficacy of cancer treatments. Therefore, we investigate the potential of using quantum dots (QDs) as drug carriers for antitumor unsymmetrical bisacridine derivatives (UAs) to cancer cells. We examine the influence of QD–UA hybrids on the cellular uptake, internalization (Confocal Laser Scanning Microscope), and the biological response (flow cytometry and light microscopy) in lung H460 and colon HCT116 cancer cells. We show the time-dependent cellular uptake of QD–UA hybrids, which were more efficiently retained inside the cells compared to UAs alone, especially in H460 cells, which could be due to multiple endocytosis pathways. In contrast, in HCT116 cells, the hybrids were taken up only by one endocytosis mechanism. Both UAs and their hybrids induced apoptosis in H460 and HCT116 cells (to a greater extent in H460). Cells which did not die underwent senescence more efficiently following QDs–UAs treatment, compared to UAs alone. Cellular senescence was not observed in HCT116 cells following treatment with both UAs and their hybrids. Importantly, QDgreen/red themselves did not provoke toxic responses in cancer or normal cells. In conclusion, QDs are good candidates for targeted UA delivery carriers to cancer cells while protecting normal cells from toxic drug activities.

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