[Preoperative bowel conditioning]. / Präoperative Konditionierung des Darms.

BACKGROUND: Gastrointestinal surgery is still associated with a relevant morbidity with the intestinal microbiome being of high importance in the pathogenesis of infectious complications. Various approaches, such as mechanical bowel preparation (MBP) with or without administration of oral antibiotics, fasting or dietary supplements aim at modulating the intestinal flora. OBJECTIVE: This review summarizes the current literature pertinent to the influence of preoperative bowel conditioning on postoperative morbidity. MATERIAL AND METHODS: A literature search was performed using the mentioned keywords with a focus on recent meta-analyses. RESULTS AND CONCLUSION: Bowel conditioning reduces postoperative infectious complications. Promising approaches are MBP plus administration of oral antibiotics, dietary supplements aiming at stabilization of the intestinal flora as well as the screening for and equilibration of malnutrition. The use of MBP as monotherapy without antibiotics should no longer be considered part of the clinical routine.

Complex role of miR-130a-3p and miR-148a-3p balance on drug resistance and tumor biology in esophageal squamous cell carcinoma.

miRNAs play a crucial role in cancer development and progression. However, results on the impact of miRNAs on drug sensitivity and tumor biology vary, and most studies to date focussed on either increasing or decreasing miRNA expression levels. Therefore, the current study investigated the role of different expression levels of miR-130a-3p and miR-148a-3p on drug resistance and tumor biology in four esophageal squamous cell carcinoma cell lines. Interestingly, up- and downregulation of both miRNAs significantly increased sensitivity towards chemotherapy. MiRNA modulation also reduced adherence and migration potential, and increased apoptosis rates. Target analyses showed that up- and downregulation of both miRNAs activated the apoptotic p53-pathway via increased expression of either BAX (miR-148a-3p) or Caspase 9 (miR-130a-3p). miR-148a-3p downregulation seemed to mediate its effects primarily via regulation of Bim rather than Bcl-2 levels, whereas we found the opposite scenario following miR-148a-3p upregulation. A similar effect was observed for miR-130a-3p regulating Bcl-2 and XIAP. Our data provide the first evidence that miRNA modulation in both directions may lead to similar effects on chemotherapy response and tumor biology in esophageal squamous cell carcinoma. Most interestingly, up- and downregulation seem to mediate their effects via modulating the balance of several validated or predicted targets.

Role of miRNAs in cell signaling of cancer associated fibroblasts.

The tumor microenvironment (TME) of cancer cells is regarded as a strong determinant for cancer development and acquisition of metastatic potential of cancer cells. Because of its influence on tumorigenesis, the TME increasingly gained attention in research within the last years. Activated fibroblasts, so-called cancer-associated fibroblasts (CAFs), which are the most prominent cell type in the stromal compartment, are responsible for the synthesis, deposition and remodeling of the extracellular matrix in tumor stroma thus creating a favorable microenvironment for cancer cells. Besides, they secrete paracrine factors, such as growth factors, chemokines and exosomes impacting on proliferation, invasion and cell signaling of cancer cells. Molecular mechanisms responsible for activation of fibroblasts and regulation of metastatic microenvironment are complex and not yet fully elucidated. However, mounting evidence suggests that miRNAs play a powerful role in the communication between cancer cells and TME. Via regulation of various signaling pathways, release of cytokines/growth factors or exosomes, miRNAs are able to regulate tumor promoting effects of CAFs. In this review, we describe baseline differences in miRNAs signatures between CAFs and normal fibroblasts and highlight the influence of miRNAs on cell signaling within CAFs.