Background Autophagy is a catabolic process for degradation of intracellular components. Damaged proteins and organelles are engulfed in double-membrane vesicles ultimately fused with lysosomes. These vesicles, known as phagophores, develop to form autophagosomes. Encapsulated components are degraded after autophagosomes and lysosomes are fused. Autophagy clears denatured proteins and damaged organelles to produce macromolecules further reused by cells. This process is vital to cell homeostasis under both physiologic and pathologic conditions. Main body While the role of autophagy in cancer is quite controversial, the majority of studies introduce it as an anti-tumorigenesis mechanism. There are evidences confirming this role of autophagy in cancer. Mutations and monoallelic deletions have been demonstrated in autophagy-related genes correlating with cancer promotion. Another pathway through which autophagy suppresses tumorigenesis is cell cycle. On the other hand, under hypoxia and starvation condition, tumors use angiogenesis to provide nutrients. Also, autophagy flux is highlighted in vessel cell biology and vasoactive substances secretion from endothelial cells. The matrix proteoglycans such as Decorin and Perlecan could also interfere with angiogenesis and autophagy signaling pathway in endothelial cells (ECs). It seems that the connection between autophagy and angiogenesis in the tumor microenvironment is very important in determining the fate of cancer cells. Conclusion Matrix glycoproteins can regulate autophagy and angiogenesis linkage in tumor microenvironment. Also, finding details of how autophagy and angiogenesis correlate in cancer will help adopt more effective therapeutic approaches.

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Background and Aim: Rheumatoid arthritis (RA) is an autoimmune inflammatory disease of unknown etiology . The chemokines and their related receptors have a pivotal role in migration and homing of leukocyte involved in the pathogenesis of RA. The goal of this study was to measure the plasma levels of CCL-17 and CCL-25 and their receptors gene (CCR4 and CCR9) expression in rheumatoid arthritis patients. Materials and Methods: 30 untreated newly diagnosed and 30 under treatment RA patients with disease modifying anti-rheumatic drugs (DMARDs) as well as 30 healthy subjects participated in this study. We assessed the gene expression of CCR4 and CCR9 by the realtime PCR method, and measured plasma levels of CCL25 and CCL17 by enzyme-linked immunosorbent assay (ELISA). Results: Comparison between control group and newly diagnosed rheumatoid arthritis patients showed significantly lower expression of CCR4 and CCR9 (P=0.047, P=0.049 respectively) in the latter group. In addition, the plasma level of CCL-25 was significantly lower in both newly diagnosed and under treatment RA patients compared to that in the healthy subjects (P=0.017, P=0.030 respectively). Conclusion:The altered expression of chemokines and their related receptors, especially those involved in the leukocyte migration to the mucosa of the gastrointestinal tract may be associated with the pathogenesis of RA.