Authors’ contributions ZAL carried out the animal experiment, XH carried out the cells experiment, WQ participated in the design of the study. LXG carried out the transmission electron Selonsertib microscopy observation. YF carried out the immunohistochemical staining. YG participated in Staurosporine the study design. CL carried out the data collection. LJ carried out the design of the study. All authors read and approved the final manuscript.”
“Background Taurolidine (TRD), a substance derived from the aminosulfoacid Taurin, was originally used in peritonitis and catheter related blood stream infections due

to its anti-microbial and anti-inflammatory properties [1–3]. Over the last years, TRD has also been shown to exert anti-neoplastic activity in vitro as well as in vivo [4]. TRD induces cell death in a variety of malignant cell lines derived from colon carcinoma [5, 6], squamous cell esophageal carcinoma [7] glioblastoma [8, 9], melanoma [10, 11], mesothelioma [12, 13] and sarcoma [14, 15]. Furthermore, first reports about systemic application of TRD in patients with gastric carcinoma and glioblastoma

revealed promising results with almost absent toxicity [16–18]. Favorable pharmacokinetics and safety profile of TRD render this compound to a promising agent in oncology [19]. However, mechanisms underlying induction of cell death by TRD are not yet fully elucidated. Among different types of programmed cell death (PCD) [20, 21], the classical apoptotic cell Selleck JAK inhibitor death has been described for TRD including the intrinsic mitochondrial [9, 12, 22–24] as well as the extrinsic death receptor

associated pathway [6, 7, 14, 24–26]. Furthermore, there seems to be a dose dependency regarding the relative contribution to apoptotic and necrotic cell death [6, 7, 9, 26, 27]. There is an ongoing discussion about the involvement of caspase activity to TRD next induced PCD. Some studies revealed enhanced caspase activity or even reversibility of TRD induced cell death by caspase-inhibition [12, 13, 15, 22, 28] whereas other denied any relevant contribution to TRD induced PCD [9, 24]. As a result, additional caspase independent forms of PCD have been suggested like autophagy or necrosis [9]. Furthermore, there is growing evidence from recent publications, that generation of reactive oxygen species (ROS) plays an important role in TRD induced PCD [9, 13, 24, 29]. However, the majority of information about TRD effects is provided from studies with one single cell line or several cell lines of one single malignancy. Methodical diversity often makes it difficult to compare results from individual cell lines and experiments. There is a lack of a comprehensive and comparative view across several cell lines of different malignancies. Furthermore, no human pancreatic cancer cell line has been evaluated for taurolidine susceptibility so far.