br Data Reported data represents the

Data Reported data represents the observed association between use of injectable insulin preceding breast cancer and the growth factor profiles at the time of cancer diagnosis in women with diabetes mellitus (Table 1). Data in Table 2 includes the observed correlations between growth factors stratified by type 2 diabetes mellitus pharmacotherapy and controls. C-peptide correlation with each of the studied growth factors is presented in Table 2, however details regarding its determination from plasma, association with cancer outcomes and use of injectable insulin has been previously reported by us [1].
Experimental design, materials and methods
Funding sources This research was funded by the following grant awards: Wadsworth Foundation Peter Rowley Breast Cancer Grant awarded to A.C.C. (UB Grant Number 55705, Contract CO26588).
Acknowledgements
Data To investigate the ability of indomethacin to induce autophagy in U251 glioma cells, we assessed its influence on intracellular acidification, expression of beclin-1, and conversion of microtubule-associated protein light chain 3 (LC3) as autophagy hallmarks [1]. Flow cytometric analysis of pH-sensitive acridine orange fluorescence revealed that indomethacin failed to increase intracellular acidification (Fig. 1A). Furthermore, the drug did not increase the expression of proautophagic protein beclin-1 or conversion of LC3-I to its lipidated, autophagosome-associated LC3-II form (Fig. 1B). Since the inability of indomethacin to augment LC3-II levels could result from the increase in LC3 degradation in autophagolysosomes [3], we analyzed LC3-II concentration in BX-795 in which autophagic proteolysis was blocked by lysosomal inhibitors chloroquine, bafilomycin A1, or ammonium chloride. While proteolysis inhibitors expectedly increased the levels of LC3-II when applied alone, no additional increase was detected in the presence of indomethacin (Fig. 1C), thus confirming its inability to increase autophagic flux. We next employed genetic and pharmacological approaches to assess the role of autophagy in indomethacin-mediated cytotoxicity to U251 cells [2]. RNA interference-mediated downregulation of autophagy-essential genes LC3 and beclin-1 (the knockdown efficiency confirmed by immunoblot in Fig. 2A) had no effect on the viability of indomethacin-treated U251 cells (Fig. 2B). Accordingly, the suppression of autophagy by proton-pump blocker bafilomycin A1, lysosomal inhibitor chloroquine, or class III phosphoinositide 3-kinase inhibitor wortmannin [3] failed to affect antiglioma effect of indomethacin (Fig. 2C).
Experimental design, materials and methods
Acknowledgments This work was supported by the Ministry of Education, Science, and Technological Development of the Republic of Serbia (grants 173053 and 41025).
Data Reported data represents the observed association between use of insulin secretagogues preceding breast cancer diagnosis and GM-CSF, G-CSF and IL-7 profiles at the time of cancer diagnosis in women with diabetes mellitus (Table 1). Data in Table 2 includes the observed correlations between the investigated biomarkers stratified by type 2 diabetes mellitus pharmacotherapy and controls. Interferon α2 and γ correlation with each of the studied biomarkers is presented in Table 2.
Experimental design, materials and methods
Funding sources This research was funded by the following grant awards: Wadsworth Foundation Peter Rowley Breast Cancer Grant awarded to A.C.C. (UB Grant Number 55705, Contract CO26588).
Acknowledgements
Data The data showed associated information on emodin against radiation induced mortality (Fig. 1), intestinal injury (Figs. 2–4), apoptosis (Fig. 3) and expression of p53 gene (Fig. 5).
Experimental design, materials and methods
Acknowledgements
Data Reported data represents the observed association between pre-existing use of injectable insulin before breast cancer diagnosis and the T-helper 1 and 2 produced cytokine profiles upon cancer diagnosis in women with both breast cancer and diabetes mellitus (Table 1). Data in Table 2 includes the observed correlations between T-helper 1 and 2 cytokines stratified by diabetes mellitus pharmacotherapy and controls.