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PIWI proteins and piRNAs primarily functions as a safeguard of germline cells by activating epigenetic regulations, silencing transposons and maintaining chromatin structure. Increasing evidences reveal that PIWI proteins and piRNAs have broader functions in many vital biological processes including cell proliferation, differentiation and survival. They have been recognized as a crucial factor in the cellular events due their role in controlling mRNA expression, turnover and translation. PIWIs, with or without its partner non-coding RNA (piRNA), govern the expression and activity of many transcription factors and signaling molecules by mastering their expression and/or post-translational modifications by directly interacting with them. In this review, we focus on the functional role of PIWI family of proteins and piRNA in physiological and pathological conditions. We compile the current knowledge about the impact of alterations of PIWI and/or piRNA on expression and activities of signaling mediators and transcriptional networks associated with cell differentiation, proliferation and survival., (Copyright © 2017. Published by Elsevier GmbH.)

CIRP has been implicated in apoptosis, yet its mechanism of action remains unknown. To determine the role of CIRP in DNA damage-induced apoptosis, we performed CIRP overexpression and knockdown experiments to investigate the effects of CIRP on key molecules in apoptosis pathway. Etoposide treatment was used to induce DNA damage-induced apoptosis. We found that CIRP knockdown increased p53 level, which in turn up-regulated pro-apoptotic genes and down-regulated anti-apoptotic genes. In contrast, CIRP overexpression decreased p53 level, which in turn down-regulated pro-apoptotic genes and up-regulated anti-apoptotic genes. The change in the expression levels of pro-apoptotic and anti-apoptotic genes shifts the balance between life and death of cells. CIRP expression is upregulated by chronic inflammation, and this phenomenon provides an interesting interventional opportunity in cancers arising from chronic inflammation. Chronic inflammation up-regulates CIRP, which in turn inhibit apoptosis. Therefore, inhibiting the function of up-regulated CIRP may have a therapeutic value in cancer., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Anaplasma phagocytophilum, the causative agent of tick-borne fever (TBF) in sheep and cattle and human granulocytic anaplasmosis, has the unique ability to selectively infect and multiply within the hostile environment of the neutrophil. Previous studies have shown that sheep with TBF are more susceptible to other infections and that infected neutrophils have reduced phagocytic ability and delayed apoptosis. This suggests that survival of A. phagocytophilum in these short-lived cells involves the ability to subvert or resist their bacterial killing, but also to modify the host cells such that the host cells survive long after infection. The present study shows that infection of sheep by A. phagocytophilum is characterized by up-regulation of some anti-apoptotic genes (BCL2, BIRC3 and CFLAR) in neutrophils and up-regulation of genes encoding the pro-inflammatory cytokines interferon-γ, interleukin (IL)-1β and IL-6 in mononuclear cells during the period of bacteraemia. Infection with A. phagocytophilum was also characterized by significant up-regulation of CYBB, which is associated with the respiratory burst of neutrophils., (Copyright © 2014 Elsevier Ltd. All rights reserved.)