Cell viability assessments of green synthesized water-soluble AgInS2/ZnS core/shell quantum dots against different cancer cell lines

2019 ◽  
Vol 34 (24) ◽  
pp. 4037-4044 ◽  
Author(s):  
Oluwatobi S. Oluwafemi ◽  
Bambesiwe M.M. May ◽  
Sundararajan Parani ◽  
Jose Varghese Rajendran
Keyword(s):  
Quantum Dots ◽  
Cell Viability ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Water Soluble ◽  
Core Shell ◽  
Image Position

Abstract

scholarly journals Pharmaceutical immunoglobulin G impairs anti-carcinoma activity of oxaliplatin in colon cancer cells

2021 ◽  
Author(s):  
Yuru Shang ◽  
Xianbin Zhang ◽  
Lili Lu ◽  
Ke Jiang ◽  
Mathias Krohn ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Viability ◽  
Cancer Patients ◽  
Cell Lines ◽  
Cancer Cell ◽  
Immunoglobulin G ◽  
Cancer Cell Lines ◽  
Human Igg ◽  
Western Blots ◽  
Igg Receptors

Abstract Background Recent evidence proves that intravenous human immunoglobulin G (IgG) can impair cancer cell viability. However, no study evaluated whether IgG application benefits cancer patients receiving chemotherapeutics. Methods Influence of pharmaceutical-grade human IgG on the viability of a series of patient-derived colon cancer cell lines with and without chemotherapeutic intervention was determined. Cell death was analysed flow cytometrically. In addition, the influence of oxaliplatin and IgG on the ERK1/2-signalling pathway was evaluated by western blots. Results We evaluated the effects of pharmaceutical IgG, such as PRIVIGEN® IgG and Tonglu® IgG, in combination with chemotherapeutics. We did not observe any significant effects of IgG on tumour cell viability directly; however, human IgG significantly impaired the anti-tumoral effects of oxaliplatin. Primary cancer cell lines express IgG receptors and accumulate human IgG intracellularly. Moreover, while oxaliplatin induced the activation of ERK1/2, the pharmaceutical IgG inhibited ERK1/2 activity. Conclusions The present study demonstrates that pharmaceutical IgG, such as PRIVIGEN® IgG and Tonglu® IgG, can impair the anti-carcinoma activity of oxaliplatin. These data strongly suggest that therapeutic IgG as co-medication might have harmful side effects in cancer patients. The clinical significance of these preclinical observations absolutely advises further preclinical, as well as epidemiological and clinical research.

scholarly journals Differential Effects of Combined ATR/WEE1 Inhibition in Cancer Cells

Cancers ◽  
2021 ◽  
Vol 13 (15) ◽  
pp. 3790
Author(s):  
Gro Elise Rødland ◽  
Sissel Hauge ◽  
Grete Hasvold ◽  
Lilli T. E. Bay ◽  
Tine T. H. Raabe ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Viability ◽  
Cancer Treatment ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Combined Treatment ◽  
Cancer Cell Lines ◽  
Variable Extent ◽  
Synergistic Induction

Inhibitors of WEE1 and ATR kinases are considered promising for cancer treatment, either as monotherapy or in combination with chemo- or radiotherapy. Here, we addressed whether simultaneous inhibition of WEE1 and ATR might be advantageous. Effects of the WEE1 inhibitor MK1775 and ATR inhibitor VE822 were investigated in U2OS osteosarcoma cells and in four lung cancer cell lines, H460, A549, H1975, and SW900, with different sensitivities to the WEE1 inhibitor. Despite the differences in cytotoxic effects, the WEE1 inhibitor reduced the inhibitory phosphorylation of CDK, leading to increased CDK activity accompanied by ATR activation in all cell lines. However, combining ATR inhibition with WEE1 inhibition could not fully compensate for cell resistance to the WEE1 inhibitor and reduced cell viability to a variable extent. The decreased cell viability upon the combined treatment correlated with a synergistic induction of DNA damage in S-phase in U2OS cells but not in the lung cancer cells. Moreover, less synergy was found between ATR and WEE1 inhibitors upon co-treatment with radiation, suggesting that single inhibitors may be preferable together with radiotherapy. Altogether, our results support that combining WEE1 and ATR inhibitors may be beneficial for cancer treatment in some cases, but also highlight that the effects vary between cancer cell lines.

Native Australian Fruit Polyphenols Inhibit Cell Viability and Induce Apoptosis in Human Cancer Cell Lines

2011 ◽  
Vol 63 (3) ◽  
pp. 444-455 ◽  
Author(s):  
Aaron Tan ◽  
Izabela Konczak ◽  
Iqbal Ramzan ◽  
Daniel Sze
Keyword(s):  
Cell Viability ◽  
Cell Lines ◽  
Cancer Cell ◽  
Human Cancer ◽  
Cancer Cell Lines ◽  
Human Cancer Cell ◽  
Human Cancer Cell Lines

Characteristics of the combination paclitaxel plus doxorubicin in breast cancer cell lines analyzed with the ATP-Cell Viability Assay

1993 ◽  
Vol 28 (1) ◽  
pp. 21-27 ◽  
Author(s):  
Ossi R. Koechli ◽  
Bernd-Uwe Sevin ◽  
James P. Perras ◽  
Ting Chao Chou ◽  
Roberto Angioli ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Viability ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines ◽  
Cell Viability Assay ◽  
Viability Assay

scholarly journals Assessment of In Vitro Bioactivities of Polysaccharides Isolated from Hericium Novae-Zealandiae

Antioxidants ◽  
2019 ◽  
Vol 8 (7) ◽  
pp. 211 ◽  
Author(s):  
Zhixia (Grace) Chen ◽  
Karen Suzanne Bishop ◽  
Hartono Tanambell ◽  
Peter Buchanan ◽  
Siew Young Quek
Keyword(s):  
Prostate Cancer ◽  
New Zealand ◽  
Cell Lines ◽  
Cancer Cell ◽  
Proliferative Activity ◽  
Prostate Cancer Cell ◽  
Cancer Cell Lines ◽  
Water Soluble ◽  
Prostate Cancer Cell Lines

The objective of this study was to investigate the potential effect of the polysaccharides isolated from Hericium novae-zealandiae, a native New Zealand fungus, on the in vitro proliferation of prostate cancer cell lines, gene expression, acetylcholinesterase (AChE) activity, and oxidation. One water-soluble and two alkali-soluble polysaccharide fractions were isolated from H. novae-zealandiae. The proliferation of the prostate cancer cell lines DU145, LNCaP, and PC3 was evaluated following treatment with these polysaccharide fractions. It was found that the polysaccharides possess anti-proliferative activity on LNCaP and PC3 cells, with a 50% growth inhibition (IC50) value as low as 0.61 mg/mL in LNCaP. Subsequently, it was determined through via RT-qPCR assay that apoptosis was one of the possible mechanisms responsible for the anti-proliferative activity in LNCaP. This was supported by the up-regulation of CASP3, CASP8, and CASP9. An alternative, discovered in PC3, was revealed to be anti-inflammation, which was hinted at by the down-regulation of IL6 and up-regulation of IL24. The polysaccharides also exhibited antioxidant and weak AChE inhibitory activities. This is the first report on the potential health benefits of polysaccharides prepared from the New Zealand fungus, H. novae-zealandiae.

High-Throughput RNA Interference Screening Identifies Synthetic Lethality Between Oncogenic KRAS Dependency and Suppression of STK33

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 3806-3806
Author(s):  
Claudia Scholl ◽  
Stefan Frohling ◽  
Ian F. Dunn ◽  
David A. Barbie ◽  
Anna C. Schinzel ◽  
...  
Keyword(s):  
Rna Interference ◽  
Protein Kinase ◽  
Cell Viability ◽  
Cell Lines ◽  
Cancer Cell ◽  
High Throughput ◽  
Synthetic Lethality ◽  
Human Cancer ◽  
Cancer Cell Lines ◽  
Dependent Manner

Abstract Activating RAS mutations are among the most common pathogenetic events in a broad spectrum of hematologic malignancies and epithelial tumors. However, oncogenic RAS has thus far not proven to be a tractable target for therapeutic intervention. An alternative to direct targeting of known oncogenes is to perform “synthetic lethality” screens to identify genes that are selectively required for cell viability in the context of specific cancer-causing mutations. Using this approach, we have discovered a synthetic lethal interaction between mutant KRAS, the most frequently mutated oncogene in human cancer, and inactivation of the gene encoding the STK33 serine/threonine protein kinase. To identify genes that are essential for cell viability in the context of mutant KRAS, we performed high-throughput loss-of-function RNA interference (RNAi) screens in eight human cancer cell lines (mutant KRAS, n=4; wildtype KRAS, n=4), representing seven different tumor types (acute myeloid leukemia, multiple myeloma, colon cancer, breast cancer, ovarian cancer, prostate cancer, glioblastoma), as well as normal human fibroblasts and mammary epithelial cells. We screened each cell line with a subset of the short hairpin RNA (shRNA) library developed by the RNAi Consortium (http://www.broad.mit.edu/genome_bio/trc/rnai.html) that consists of 5,024 individual shRNA constructs targeting 1,011 human genes, including the majority of known and putative protein kinase and phosphatase genes and a selection of known cancer-related genes. In these cell lines, suppression of STK33 preferentially inhibited the viability and proliferation of cells that were dependent on mutant KRAS. The differential requirement for STK33 based on oncogenic KRAS dependency was confirmed in 16 additional cell lines using in vitro transformation assays and human tumor xenograft models. Biochemical analyses support the hypothesis that STK33 promotes cell growth and survival in a kinase activity-dependent manner by regulating the activity of S6K1 as well as BAD-induced apoptosis selectively in mutant KRAS-dependent cells. Notably, molecular genetic characterization of cancer cell lines and analysis of patient-derived genomic data sets indicate that STK33 is not frequently mutated or overexpressed in human tumors. These observations identify STK33 as a potential target for the treatment of mutant KRAS-driven cancers that may have a broad therapeutic index in normal versus malignant cells, and illustrate the potential of RNAi for discovering critical functional dependencies created by oncogenic mutations that cannot be identified using other genomic technologies.

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