An Aptamer Bio-barCode (ABC) assay using SPR, RNase H, and probes with RNA and gold-nanorods for anti-cancer drug screening

The Analyst ◽  
2017 ◽  
Vol 142 (19) ◽  
pp. 3579-3587 ◽  
Author(s):  
Jacky Fong-Chuen Loo ◽  
Chengbin Yang ◽  
Hing Lun Tsang ◽  
Pui Man Lau ◽  
Ken-Tye Yong ◽  
...  
Keyword(s):  
Cell Death ◽  
Cancer Cells ◽  
Gold Nanorods ◽  
Drug Screening ◽  
Rnase H ◽  
Cancer Drug ◽  
Next Generation ◽  
Anti Cancer ◽  
A Cell

We have developed a next generation aptamer-based bio-barcode (ABC) assay to detect cytochrome-c (Cyto-c), a cell death marker released from cancer cells, for anti-cancer drug screening.

scholarly journals Effects of light-activated diazido-Pt IV complexes on cancer cells in vitro

2013 ◽  
Vol 371 (1995) ◽  
pp. 20120118 ◽  
Author(s):  
Patrick J. Bednarski ◽  
Katharina Korpis ◽  
Aron F. Westendorf ◽  
Steffi Perfahl ◽  
Renate Grünert
Keyword(s):  
Cell Death ◽  
Cancer Cells ◽  
Calf Thymus Dna ◽  
Cross Resistance ◽  
Cancer Drug ◽  
Cancer Cell Growth ◽  
Calf Thymus ◽  
Anti Cancer ◽  
Cellular Dna

Various Pt IV diazides have been investigated over the years as light-activatable prodrugs that interfere with cell proliferation, accumulate in cancer cells and cause cell death. The potencies of the complexes vary depending on the substituted amines (pyridine=piperidine>ammine) as well as the coordination geometry ( trans diazide> cis ). Light-activated Pt IV diazides tend to be less specific than cisplatin at inhibiting cancer cell growth, but cells resistant to cisplatin show little cross-resistance to Pt IV diazides. Platinum is accumulated in the cancer cells to a similar level as cisplatin, but only when activated by light, indicating that reactive Pt species form photolytically. Studies show that Pt also becomes attached to cellular DNA upon the light activation of various Pt IV diazides. Structures of some of the photolysis products were elucidated by LC–MS/MS; monoaqua- and diaqua-Pt II complexes form that are reactive towards biomolecules such as calf thymus DNA. Platination of calf thymus DNA can be blocked by the addition of nucleophiles such as glutathione and chloride, further evidence that aqua-Pt II species form upon irradiation. Evidence is presented that reactive oxygen species may be generated in the first hours following photoactivation. Cell death does not take the usual apoptotic pathways seen with cisplatin, but appears to involve autophagy. Thus, photoactivated diazido-Pt IV complexes represent an interesting class of potential anti-cancer agents that can be selectively activated by light and kill cells by a mechanism different to the anti-cancer drug cisplatin.

scholarly journals Chitosan-Modified Silver Nanoparticles Enhance Cisplatin Activity in Breast Cancer Cells

2020 ◽  
Vol 11 (3) ◽  
pp. 10572-10584
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Therapeutic Potential ◽  
Cancer Drug ◽  
Breast Cancer Cell Lines ◽  
Anti Cancer ◽  
Silver Nps ◽  
Sensitivity Specificity

Cancer therapy has been hindered by treatments lacking sensitivity, specificity, and affordability. The side effects of conventional chemotherapy enforce the need for a treatment strategy that would maximize the anti-cancer activity of the drug while minimizing its’ adverse effects on healthy cells. Nanoparticles (NPs) as carriers for anti-cancer drugs have attracted interest due to their favorable properties, which include the enhanced permeability and retention effect. Silver NPs (AgNPs) have been explored as nanocarriers owing to their good conductivity, chemical stability, and therapeutic potential. In this study, AgNPs were synthesized, functionalized with chitosan (CS), and loaded with the anti-cancer drug cisplatin (CIS). Successful conjugation, size distribution, and morphology of the NPs were assessed by UV-vis and Fourier transform infra-red (FTIR) spectroscopy, NP tracking analysis (NTA), and transmission electron microscopy (TEM). The encapsulated CIS (>80%) was efficiently and rapidly released from the nanocomplex at low pH, favoring delivery to a tumor micro-environment. Cytotoxicity profiles of the CS-AgNP-CIS nanocomplexes exhibited significant cell death in the human breast cancer cell lines, MCF-7 and SKBR-3. They were more effective than the free drug, exhibiting >50% cell death. Our results demonstrate a potentially efficient anti-cancer drug delivery system with selectivity to breast cancer cells.

scholarly journals A cell-loss-free concave microwell array based size-controlled multi-cellular tumoroid generation for anti-cancer drug screening

PLoS ONE ◽  
2019 ◽  
Vol 14 (7) ◽  
pp. e0219834 ◽  
Author(s):  
Sang Woo Lee ◽  
Soo Yeon Jeong ◽  
Tae Hoon Shin ◽  
Junhong Min ◽  
Donghyun Lee ◽  
...  
Keyword(s):  
Drug Screening ◽  
Cell Loss ◽  
Cancer Drug ◽  
Microwell Array ◽  
Anti Cancer ◽  
A Cell ◽  
Size Controlled

scholarly journals Differential Mechanisms of Cell Death Induced by HDAC Inhibitor SAHA and MDM2 Inhibitor RG7388 in MCF-7 Cells

Cells ◽  
2018 ◽  
Vol 8 (1) ◽  
pp. 8 ◽  
Author(s):  
Umamaheswari Natarajan ◽  
Thiagarajan Venkatesan ◽  
Vijayaraghavan Radhakrishnan ◽  
Shila Samuel ◽  
Appu Rathinavelu
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cell Death ◽  
Cancer Cells ◽  
Hdac Inhibitor ◽  
The Other ◽  
Combination Treatments ◽  
Cycle Arrest ◽  
Anti Cancer ◽  
Mcf 7

Gene expression is often altered by epigenetic modifications that can significantly influence the growth ability and progression of cancers. SAHA (Suberoylanilide hydroxamic acid, also known as Vorinostat), a well-known Histone deacetylase (HDAC) inhibitor, can stop cancer growth and metastatic processes through epigenetic alterations. On the other hand, Letrozole is an aromatase inhibitor that can elicit strong anti-cancer effects on breast cancer through direct and indirect mechanisms. A newly developed inhibitor, RG7388 specific for an oncogene-derived protein called MDM2, is in clinical trials for the treatment of various cancers. In this paper, we performed assays to measure the effects of cell cycle arrest resulting from individual drug treatments or combination treatments with SAHA + letrozole and SAHA + RG7388, using the MCF-7 breast cancer cells. When SAHA was used individually, or in combination treatments with RG7388, a significant increase in the cytotoxic effect was obtained. Induction of cell cycle arrest by SAHA in cancer cells was evidenced by elevated p21 protein levels. In addition, SAHA treatment in MCF-7 cells showed significant up-regulation in phospho-RIP3 and MLKL levels. Our results confirmed that cell death caused by SAHA treatment was primarily through the induction of necroptosis. On the other hand, the RG7388 treatment was able to induce apoptosis by elevating BAX levels. It appears that, during combination treatments, with SAHA and RG7388, two parallel pathways might be induced simultaneously, that could lead to increased cancer cell death. SAHA appears to induce cell necroptosis in a p21-dependent manner, and RG7388 seems to induce apoptosis in a p21-independent manner, outlining differential mechanisms of cell death induction. However, further studies are needed to fully understand the intracellular mechanisms that are triggered by these two anti-cancer agents.

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