	3.	Woźniak A., Walawender M., Tempka D., Coy E., Załęski K., Grześkowiak B., Mrówczyński R.
		In vitro genotoxicity and cytotoxicity of polydopamine-coated magnetic nanostructures Synthesis of magnetic nanoparticles and magnetic nanoclusters was performed by the co-precipitation method or solvothermal synthesis, respectively, followed by oxidative polymerization of dopamine, resulting in a polydopamine (PDA) shell. The nanomaterials obtained were described using TEM, FTIR and magnetic measurements. For the first time, cyto- and genotoxicity studies of polydopamine-coated nanostructures were performed on cancer and normal cell lines, providing in-depth insight into the toxicity of such materials. The tests conducted, e.g. ROS, apoptosis and DNA double-break of the nanomaterials obtained revealed the low toxicity of these structures. Thus, these results prove the biocompatibility and low genotoxicity of these materials and provide new data on the toxicity of PDA-coated materials, which is of great importance for their biomedical application. © 2017 Elsevier Ltd
		Toxicology in Vitro, 44, 256-265 (2017)
		DOI: 10.1016/j.tiv.2017.07.022 (Pobrane: 2023-02-08)

	2.	Boś-Liedke A. Walawender M., Woźniak A., Flak D., Gapiński J., Jurga S., Kucińska M., Plewiński A., Murias M., Elewa M., Lampp L., Imming P., Tadyszak K.
		EPR oximetry sensor-developing a TAM derivative for in vivo studies Oxygenation is one of the most important physiological parameters of biological systems. Low oxygen concentration (hypoxia) is associated with various pathophysiological processes in different organs. Hypoxia is of special importance in tumor therapy, causing poor response to treatment. Triaryl methyl (TAM) derivative radicals are commonly used in electron paramagnetic resonance (EPR) as sensors for quantitative spatial tissue oxygen mapping. They are also known as magnetic resonance imaging (MRI) contrast agents and fluorescence imaging compounds. We report the properties of the TAM radical tris(2,3,5,6-tetrachloro-4-carboxy-phenyl)methyl, (PTMTC), a potential multimodal (EPR/fluorescence) marker. PTMTC was spectrally analyzed using EPR and characterized by estimation of its sensitivity to the oxygen in liquid environment suitable for intravenous injection (1mM PBS, pH=7.4). Further, fluorescent emission of the radical was measured using the same solvent and its quantum yield was estimated. An in vitro cytotoxicity examination was conducted in two cancer cell lines, HT-29 (colorectal adenocarcinoma) and FaDu (squamous cell carcinoma) and followed by uptake studies. The stability of the radical in different solutions (PBS pH=7.4, cell media used for HT-29 and FaDu cells culturing and cytotoxicity procedure, full rat blood and blood plasma) was determined. Finally, a primary toxicity test of PTMTC was carried out in mice. Results of spectral studies confirmed the multimodal properties of PTMTC. PTMTC was demonstrated to be not absorbed by cancer cells and did not interfere with luciferin-luciferase based assays. Also in vitro and in vivo tests showed that it was non-toxic and can be freely administrated till doses of 250 mg/kg BW via both i.v. and i.p. injections. This work illustrated that PTMTC is a perfect candidate for multimodal (EPR/fluorescence) contrast agent in preclinical studies.
		Cell Biochemistry and Biophysics, , 1-10 (2017)
		DOI: 10.1007/s12013-017-0824-3 (Pobrane: 2020-10-23)

	1.	Ciesla M., Marona P., Kozakowska M., Jez M., Seczynska M., Loboda A., Bukowska-Strakova K., Szade A., Walawender M., Stepniewski J., Szade K.
		Heme oxygenase-1 controls an HDAC4-MIR-206 pathway of oxidative stress in rhabdomyosarcoma Rhabdomyosarcoma (RMS) is an aggressive soft tissue cancer characterized by disturbed myogenic differentiation. Here we report a role for the oxidative stress response factor HO 1 in progression of RMS. We found that HO 1 was elevated and its effector target miR 206 decreased in RMS cell lines and clinical primary tumors of the more aggressive alveolar phenotype (aRMS). In embryonal RMS (eRMS), HO 1 expression was induced by Pax3/7 FoxO1, an aRMS hallmark oncogene, followed by a drop in miR 206 levels. Inhibition of HO 1 by tin protoporphyrin (SnPP) or siRNA downregulated Pax3/7 FoxO1 target genes and induced a myogenic program in RMS. These effects were not mediated by altered myoD expression; instead, cells with elevated HO 1 produced less reactive oxygen species, resulting in nuclear localization of HDAC4 and miR 206 repression. HO 1 inhibition by SnPP reduced growth and vascularization of RMS tumors in vivo accompanied by induction of miR 206. Effects of SnPP on miR 206 expression and RMS tumor growth were mimicked by pharmacologic inhibition of HDAC. Thus, HO 1 inhibition activates an miR 206-dependent myogenic program in RMS, offering a novel therapeutic strategy for treatment of this malignancy. © 2016 AACR.
		Cancer Research, 76(19), 5707-5718 (2016)
		DOI: 10.1158/0008-5472.CAN-15-1883 (Pobrane: 2022-10-13)