Abstract
Cytokines are secreted by various cell types and act as critical mediators in many physiological processes, including immune response and tumor progression. Cytokines production is precisely and timely regulated by multiple mechanisms at different levels, ranging from transcriptional to post-transcriptional and posttranslational processes. Monocyte chemoattractant protein-1 induced protein 1 (MCPIP1), a potent immunosuppressive protein, was first described as a transcription factor in monocytes treated with monocyte chemoattractant protein-1 (MCP-1) and subsequently found to possess intrinsic RNase and deubiquitinase activities. MCPIP1 tightly regulates cytokines expression via various functions. Furthermore, cytokines such as interleukin 1 beta (IL-1B) and MCP-1 and inflammatory cytokines inducer lipopolysaccharide (LPS) strongly induce MCPIP1 expression. Mutually regulated MCPIP1 and cytokines form a complicated network in the tumor environment. In this review, we summarize how MCPIP1 and cytokines reciprocally interact and elucidate the effect of the network formed by these components in cancer-related immunity with aim of exploring potential clinical benefits of their mutual regulation.
Highlights
Cytokines are secreted by various cell types and act as critical mediators in many physiological processes, including immune response and tumor progression
Monocyte chemoattractant protein-1 induced protein 1 (MCPIP1), a potent immunosuppressive protein, was first described as a transcription factor in monocytes treated with monocyte chemoattractant protein-1 (MCP-1) and subsequently found to possess intrinsic RNase and deubiquitinase activities
Various cell types and multiple mechanisms participate in the tight regulation of cytokines production
Summary
The idea that inflammation contributes to the onset of cancer, which is well accepted and considered a vital characteristic of cancer, can be traced back to the 19th century (Coussens et al, 2013; Elinav et al, 2013; Coffelt and De Visser, 2014; Maman and Witz, 2018). Huang et al showed that MCPIP1 inhibited proinflammatory cytokines production by negatively regulated LPS-induced JNK signaling. A massive number of studies have shown that MCPIP1 can directly target and degrade proinflammatory cytokines transcripts, acting as a negative regulator of inflammation. USP10 knockdown rescued MCPIP1mediated repression of DNA damage-induced inflammatory cytokine production Their results showed that MCPIP1 can affect DNA damage signaling in cells after genotoxic treatment. Studies in breast cancer showed that MCPIP1 directly binds and cleaves the mRNAs of multiple antiapoptotic genes, such as BCL2A1, BCL2L1, and RELB, and subsequently induces tumor cells apoptosis (Lu et al, 2016). Overexpression of MCPIP1 downregulated miR3613-3p expression in neuroblastoma cells, which upregulates apoptotic protease activating factor 1 (APAF1), causing cells apoptosis by caspase-9 proteolysis (Boratyn et al, 2016) Limitless proliferation is another vital hallmark of cancer. Determining how to interfere with MCPIP1 expression in cancer cells or immune cells is a major challenge for translating research findings to clinical practice
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
