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Objective: The primary objective was to study whether the cytotoxicity of Wortmannin (Wtmn) triggers apoptotic programmed cell death on the widely-used model breast cancer MCF-7 cell to understand this small molecule’s biological signaling mechanisms. Methods: In this present study, MCF-7 cells anti-proliferative activities determined by using MTT assays to quantify the cytotoxicity of the Wtmn. The direct cellular and molecular effect of Wtmn was investigated selectively using flow cytometric cell cycle, mitochondrial membrane potential (MMP) assays, fluorescent and phase contrast microscopy. Results: Our biochemical and morphological experimental analysis showed that Wtmn inhibits the proliferation of MCF-7 breast cancer cells and facilitates their entry into the apoptosis mode of programmed cell death. Conclusion: Our experimental results directed towards elucidating the cytotoxicity of Wtmn and it’s biological mechanisms indicates anti-proliferative and apoptogenic properties. This strategy can serve as a screening model for anti-cancer treatment in-vitro.

Rozina Akter,1 Md. Zakir Hossain,2 Maurice G Kleve,3 Michael A Gealt31Applied Biosciences Emphasis, Department of Applied Science, 2Graduate Institute of Technology, 3Department of Biology, College of Science and of Mathematics, University Arkansas at Little Rock, Little Rock, AR, USABackground: Apoptosis can be used as a reliable marker for evaluating potential chemotherapeutic agents. Because wortmannin is a microbial steroidal metabolite, it specifically inhibits the phosphatidyl inositol 3-kinase pathway, and could be used as a promising apoptosis-based therapeutic agent in the treatment of cancer. The objective of this study was to investigate the biomolecular mechanisms involved in wortmannin-induced cell death of breast cancer-derived MCF-7 cells.Methods and results: Our experimental results demonstrate that wortmannin has strong apoptotic effects through a combination of different actions, including reduction of cell viability in a dose-dependent manner, inhibition of proliferation, and enhanced generation of intracellular reactive oxygen species.Conclusion: Our findings suggest that wortmannin induces MCF-7 cell death via a programmed pathway showing chromatin condensation, nuclear fragmentation, reactive oxygen species, and membrane blebbing, which are characteristics typical of apoptosis.Keywords: wortmannin, human breast adenocarcinoma, apoptosis, reactive oxygen species, flow cytometry

Cytotoxicity study of magnetic nanomaterials is a key consideration for biomedical applications. Very little is known about the cytotoxic and anti-cancer effects of nickel nanowires (Ni NWs) on mammalian cells and their interaction with proliferating cancer cells. Current therapeutics do not address the full heterogeneity of pancreatic cancers due to the resistance to apoptosis and does not suffice for a successful treatment. Therefore, synthesis of novel anticancer drugs continues to be a potential topic for pancreatic cancer research. In this study, we have investigated the cellular toxicity and anti-cancer effects of Ni NWs in one of the most aggressive human pancreatic ductal cancer (Panc-1) cell lines with the objective of development of a potential treatment strategy. Ni NWs were fabricated in a custom-made setup utilizing the electrodeposition method. Elemental analysis, crystallographic structure, and morphological properties of the synthesized Ni NWs were investigated using Energy Dispersive X-ray Analysis (EDAX), X-Ray Diffraction (X-RD) and Scanning Electron Microscopy (SEM), respectively. Panc-1 cell cultures were maintained according to a slightly modified American Type Culture Collection (ATCC) protocol. Morphological apoptogenic characteristics assessment of the Ni NWs induced Panc-1 cell was accomplished using phase contrast microscopy (PCM). Two commercially available cytotoxicity procedures including 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide (MTT) and trypan blue (TB) assays were utilized to determine the qualitative and quantitative cytotoxicity and anti-cancer effects of Ni NWs. As a negative control, Panc-1 cells without Ni NWs treatment were used in all experiments. Phase contrast microscopy (PCM) was used to confirm the Ni NWs internalization by Panc-1 cells. Both the MTT and TB assays, qualitatively and quantitatively confirmed the cytotoxic and anti-cancer effects of Ni NWs treated Panc-1 cells in vitro in both concentration and exposure-time dependent manners. We studied the cytotoxic and anti-cancer effects of Ni NWs on Panc-1 cells using novel integrated bionanotechnological approaches to understand the corresponding biological pathway with the objective of developing pancreatic cancer treatment. More specifically, we explored the molecular mechanisms associated with the pathway involved in Ni NWs induced toxicity against Panc-1 cells. Our results demonstrated that Ni NWs show strong candidacy for targeting cell selective applications in pancreatic cancer therapy. Key words: Nickel Nanowires, anti-cancer effects, pancreatic cancer.