How are MCPIP1 and cytokines mutually regulated in cancer-related immunity?

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.

Mitochondrial DNA mutations and aminoglycoside antibiotics and hearing loss / 临床耳鼻咽喉头颈外科杂志

Mitochondrial DNA mutations are one of the most important causes of sensorineural hearing loss. A1555G and C1494T mutations of mitochondrial 12S rRNA gene are the molecular basis for aminoglycoside hyper- sensitivity and can lead to aminoglycoside-induced hearing loss. Primary mutations in tRNA such as tRNA(Ser(UCN))7472insC are associated with syndromic hearing loss. While other mutations such as tRNA"(Se(UCN) )G7444A were considered synergy with the primary RNA mutations, modulating the phenotypic manifestation. This review de- scribes a detailed summary of hearing loss associated with mtDNA mutations and/or aminoglycoside antibiotics, and provides the possible molecular mechanisms in deafness expression.