Oncoprotein SND1 induces ER-associated degradation for nascent MHC-I heavy chain, leading to impaired CD8 ⁺ T cell response in tumor.

Autism Spectrum Disorder (ASD) is a collective term for neurodevelopmental disorders with core features of social communication impairment, restricted and repetitive behaviors, and narrow interests. These include classic autism, Asperger’s syndrome, and pervasive developmental disorder not otherwise specified. ASD is currently managed with behavioral interventions, rehabilitation training, and family support, but there is no curative medication. Recent studies suggest that some patients with ASD may experience gastrointestinal symptoms. Perhaps this is associated with the disturbances of gut microbiota. Increasing evidence has demonstrated that the composition of gut microbiota in ASD individuals is different from that in normal population and may be associated with neurodevelopmental processes via the gut–brain axis. This article reviews the evidence for the association between gut microbiota and ASD, describes the characteristics of microbial changes, and analyzes the mechanism by which changes in the composition of the microbiota affect the occurrence and development of ASD. Finally, we review recent advances in microbiota-targeted therapeutic strategies, including probiotics, prebiotics, and fecal microbiota transplantation, which provide new approaches to alleviate and improve autism-related symptoms and point out the future research direction.

Platinum-based (especially cisplatin) chemotherapy is the main treatment after surgery for ovarian cancer. Although the initial treatment is effective, chemotherapy resistance develops rapidly. Therefore, chemotherapy resistance has always been a huge obstacle in the treatment of ovarian cancer. SND1 is an evolutionarily conserved multifunctional protein that plays a role in promoting tumorigenesis under various stress states. In this study, SKOV3 ovarian cancer cells deficient in SND1 were observed to be more apoptotic and to express more apoptotic protein after treatment with cisplatin, while cells overexpressing SND1 exhibited a decreased number of apoptotic cells and expression of apoptotic proteins. Moreover, SND1 can regulate the expression of GAS6 and then activate the AKT signaling pathway to achieve the regulation of sensitivity to cisplatin-induced apoptosis for ovarian cancer.