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.

Synthesis, biological evaluation, substitution behaviour and DFT study of Pd(ii) complexes incorporating benzimidazole derivative

2018 ◽  
Vol 42 (4) ◽  
pp. 2574-2589 ◽  
Author(s):  
Ishani Mitra ◽  
Subhajit Mukherjee ◽  
Venkata P. Reddy B. ◽  
Bashkim Misini ◽  
Payel Das ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Benzimidazole Derivative ◽  
Biological Evaluation ◽  
Dft Study ◽  
Binding Ability ◽  
Normal Cells ◽  
Bsa Binding ◽  
Reduced Toxicity

Pd(ii) complexes with good DNA/BSA binding ability exhibit cytotoxicity comparable to cisplatin on different cancer cells along with reduced toxicity towards normal cells.

A novel water-soluble fluorescent probe with ultra-sensitivity over a wider pH range and its application for differentiating cancer cells from normal cells

The Analyst ◽  
2019 ◽  
Vol 144 (23) ◽  
pp. 6975-6980 ◽  
Author(s):  
Zilu Li ◽  
Chen Yu ◽  
Yanan Chen ◽  
Zihan Zhuang ◽  
Bin Tian ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Fluorescent Probe ◽  
Water Soluble ◽  
Normal Cells ◽  
Ph Range

A water-soluble fluorescent probe with ultra-sensitivity over a wider pH range was developed to differentiate cancer cells from normal cells.

scholarly journals Molecular Decoy to the Y-Box Binding Protein-1 Suppresses the Growth of Breast and Prostate Cancer Cells whilst Sparing Normal Cell Viability

PLoS ONE ◽  
2010 ◽  
Vol 5 (9) ◽  
pp. e12661 ◽  
Author(s):  
Jennifer H. Law ◽  
Yvonne Li ◽  
Karen To ◽  
Michelle Wang ◽  
Arezoo Astanehe ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Viability ◽  
Cancer Cells ◽  
Normal Cell ◽  
Binding Protein ◽  
Prostate Cancer Cells ◽  
Breast And Prostate Cancer

Targeting Y397 FAK scaffolding compared with FAK kinase inhibition: Efficacy and specificity for tumor cells.

2013 ◽  
Vol 31 (15_suppl) ◽  
pp. e13547-e13547 ◽  
Author(s):  
Vita Golubovskaya ◽  
Baotran Ho ◽  
Adam Stright ◽  
Maria Zajac-Kaye ◽  
Steven N. Hochwald ◽  
...  
Keyword(s):  
Cell Viability ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Kinase Domain ◽  
Normal Cells ◽  
Atp Binding Site ◽  
Survival Signaling ◽  
Student’S T

e13547 Background: Focal Adhesion Kinase is a non-receptor kinase which is highly overexpressed and activated or autophosphorylated in many types of tumors and plays a major role in survival signaling and metastasis. Recently, our group developed a highly specific allosteric scaffolding FAK autophosphorylation inhibitor, Y15, that blocked FAK Y397 autophosphorylation, decreased cancer cell viability, and significantly decreased breast, neuroblastoma, pancreatic and glioblastoma tumor growth. In addition, Y15 was not toxic in mice. In this study, we compared side by side efficacy of Y15 with two other FAK inhibitors in clinical trials, Pfizer PF-04554878 and Glaxo GSK-2256098. Methods: MTT, clonogenicity and Western blotting assays were used to detect the effect of FAK inhibitors on different cancer and normal cells. Student’s t-test was used for statistical analysis and p<0.05 was considered significant. Results: We tested different cancer cell lines: kidney 293T, colon SW620 and LoVo; lung A549; glioblastoma U251 and U87; breast: BT474, MDA-231, MDA-361, MDA-453, MDA-468 and T47D and pancreatic PANC-1 cancer cells with different doses of Y15, PF and GSK inhibitors by MTT assay and found that Y15 was the most effective at decreasing cancer cell viability in most cancer cell lines, with higher efficacy than PF and much higher efficacy than GSK inhibitor. The same was observed for clonogenicity assay. In addition, we found that Y15 did not significantly affect viability of normal colon (CCD-112) cells, while viability of these cells with PF and GSK decreased to 54% and 57% at a 2 microM dose, respectively, from 100% in untreated cells. In addition, Y15 significantly decreased Y397-FAK, Y418-Src, phospho- Ser 473-AKT and phospho-ERK1/2, while PF had less effect and GSK only a minimal effect in four different cancer cell lines: U251, A549, 293T and Lovo at 10 microM and 100 microM doses, showing high potency of the FAK Y397 scaffolding inhibitor. Conclusions: These data show that Y15, which inhibits the Y397 site of FAK, is more potent against cancer cells and less toxic to normal cells than FAK inhibitors that target the conserved ATP-binding site in the kinase domain.

scholarly journals Essential oil loaded pectin/chitosan nanoparticles preparation and optimization via Box–Behnken design against MCF-7 breast cancer cell lines

RSC Advances ◽  
2020 ◽  
Vol 10 (15) ◽  
pp. 8703-8708 ◽  
Author(s):  
Olivia A. Attallah ◽  
Amro Shetta ◽  
Fatma Elshishiny ◽  
Wael Mamdouh
Keyword(s):  
Breast Cancer ◽  
Essential Oil ◽  
Cell Viability ◽  
Cancer Cells ◽  
Chitosan Nanoparticles ◽  
Fold Increase ◽  
Breast Cancer Cell Lines ◽  
Normal Cells ◽  
Box Behnken Design ◽  
Mcf 7

Pec/CS/JO formulated nanocomposite showed a 13-fold increase in potency against cancer cells, whereas cell viability of normal cells wasn't affected.

Facile synthesis of mercaptosuccinic acid-capped CdTe/CdS/ZnS core/double shell quantum dots with improved cell viability on different cancer cells and normal cells

2016 ◽  
Vol 18 (11) ◽  
Author(s):  
Sundararajan Parani ◽  
Giridharan Bupesh ◽  
Elayaperumal Manikandan ◽  
Kannaiyan Pandian ◽  
Oluwatobi Samuel Oluwafemi
Keyword(s):  
Quantum Dots ◽  
Cell Viability ◽  
Cancer Cells ◽  
Facile Synthesis ◽  
Normal Cells ◽  
Mercaptosuccinic Acid

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 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.

Ca2+ movement and cytotoxicity induced by the pyrethroid pesticide bifenthrin in human prostate cancer cells

2019 ◽  
Vol 38 (10) ◽  
pp. 1145-1154 ◽  
Author(s):  
J-M Chien ◽  
W-Z Liang ◽  
W-C Liao ◽  
C-C Kuo ◽  
C-T Chou ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Endoplasmic Reticulum ◽  
Cell Viability ◽  
Cancer Cells ◽  
Water Soluble ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells ◽  
Fura 2 ◽  
Pyrethroid Pesticide

Bifenthrin, a commonly used pyrethroid pesticide, evokes various toxicological effects in different models. However, the effect of bifenthrin on cytosolic-free Ca2+ level ([Ca2+] i) and cytotoxicity in human prostate cancer cells is unclear. This study examined whether bifenthrin altered Ca2+ homeostasis and cell viability in PC3 human prostate cancer cells. [Ca2+] i in suspended cells were measured using the fluorescent Ca2+-sensitive dye fura-2. Cell viability was examined by 4-[3-[4-lodophenyl]-2-4(4-nitrophenyl)-2H-5-tetrazolio-1,3-benzene disulfonate] water soluble tetrazolium-1 assay. Bifenthrin (100–400 μM) concentration-dependently induced [Ca2+] i rises. Ca2+ removal reduced the signal by approximately 30%. In Ca2+-free medium, treatment with the endoplasmic reticulum Ca2+ pump inhibitor 2,5-di-tert-butylhydroquinone (BHQ) abolished bifenthrin-evoked [Ca2+] i rises. Conversely, treatment with bifenthrin abolished BHQ-evoked [Ca2+] i rises. Inhibition of phospholipase C (PLC) with U73122 significantly inhibited bifenthrin-induced [Ca2+] i rises. Mn2+ has been shown to enter cells through similar mechanisms as Ca2+ but quenches fura-2 fluorescence at all excitation wavelengths. Bifenthrin (400 μM)-induced Mn2+ influx implicates that Ca2+ entry occurred. Bifenthrin-induced Ca2+ entry was inhibited by 30% by protein kinase C (PKC) activator (phorbol 12-myristate 13 acetate) and inhibitor (GF109203X) and three inhibitors of store-operated Ca2+ channels: nifedipine, econazole, and SKF96365. Bifenthrin at 175–275 μM decreased cell viability, which was not reversed by pretreatment with the Ca2+ chelator 1,2-bis(2-aminophenoxy) ethane- N, N, N′, N′-tetra acetic acid-acetoxymethyl ester. Together, in PC3 cells, bifenthrin-induced [Ca2+] i rises by evoking PLC-dependent Ca2+ release from the endoplasmic reticulum and Ca2+ entry via PKC-sensitive store-operated Ca2+ entry. Bifenthrin also caused Ca2+-independent cell death.

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