Translation is a fundamental process in all living organisms that involves the decoding of genetic information in mRNA by ribosomes and translation factors. The dysregulation of mRNA translation is a common feature of tumorigenesis. Protein expression reflects the total outcome of multiple regulatory mechanisms that change the metabolism of mRNA pathways from synthesis to degradation. Accumulated evidence has clarified the role of an increasing amount of mRNA modifications at each phase of the pathway, resulting in translational output. Translation machinery is directly affected by mRNA modifications, influencing translation initiation, elongation, and termination or altering mRNA abundance and subcellular localization. In this review, we focus on the translation initiation factors associated with cancer as well as several important RNA modifications, for which we describe their association with cancer.
BackgroundAccumulating evidence suggests that alterations in gut microbiota composition and diversity are associated with Atopic dermatitis (AD). But until now, the causal association between them has been unclear.MethodsWe employed a two-sample Mendelian Randomization (MR) study to estimate the potential causality of gut microbiota on AD risk. The summary statistics related to the gut microbiota were obtained from a large-scale genome-wide genotype and 16S fecal microbiome dataset from 18,340 individuals (24 cohorts) analyzed by the MiBioGen Consortium, comprising 211 gut microbiota. AD data were also derived from strictly defined AD data collected by FinnGen biobank analysis, which included 218,467 European ancestors (5,321 AD patients and 213,146 controls). The inverse variance weighted method (IVW), weighted median (WME), and MR-Egger were used to determine the changes of AD pathogenic bacterial taxa, followed by sensitivity analysis including horizontal pleiotropy analysis, Cochran’s Q test, and the leave-one-out method to assess the reliability of the results. In addition, MR Steiger’s test was used to test the suppositional relationship between exposure and outcome.ResultsA total of 2,289 SNPs (p < 1 × 10−5) were included, including 5 taxa and 17 bacterial characteristics (1 phylum, 3 classes, 1 order, 4 families, and 8 genera), after excluding the IVs with linkage disequilibrium (LD). Combining the analysis of the results of the IVW models, there were 6 biological taxa (2 families, and 4 genera) of the intestinal flora positively associated with the risk of AD and 7 biological taxa (1 phylum, 2 classes, 1 order, 1 family, and 2 genera) of the intestinal flora negatively associated. The IVW analysis results showed that Tenericutes, Mollicutes, Clostridia, Bifidobacteriaceae, Bifidobacteriales, Bifidobacterium, and Christensenellaceae R 7 group were negatively correlated with the risk of AD, while Clostridiaceae 1, Bacteroidaceae, Bacteroides, Anaerotruncus, the unknown genus, and Lachnospiraceae UCG001 showed the opposite trend. And the results of the sensitivity analysis were robust. MR Steiger’s test showed a potential causal relationship between the above intestinal flora and AD, but not vice versa.ConclusionThe present MR analysis genetically suggests a causal relationship between changes in the abundance of the gut microbiota and AD risk, thus not only providing support for gut microecological therapy of AD but also laying the groundwork for further exploration of the mechanisms by which the gut microbiota contributes to the pathogenesis of AD.
IntroductionThe gut-brain axis has been widely recognized in autism spectrum disorder (ASD), and probiotics are considered to potentially benefit the rescuing of autism-like behaviors. As a probiotic strain, Lactiplantibacillus plantarumN-1(LPN-1) was utilized to investigate its effects on gut microbiota and autism-like behaviors in ASD mice constructed by maternal immune activation (MIA).MethodsAdult offspring of MIA mice were given LPN-1 at the dosage of 2 × 109 CFU/g for 4 weeks before subject to the behavior and gut microbiota evaluation.ResultsThe behavioral tests showed that LPN-1 intervention was able to rescue autism-like behaviors in mice, including anxiety and depression. In which the LPN-1 treatment group increased the time spent interacting with strangers in the three-chamber test, their activity time and distance in the central area increased in the open field test, and their immobility time decreased when hanging their tails. Moreover, the supplementation of LPN-1 reversed the intestinal flora structure of ASD mice by enhancing the relative abundance of the pivotal microorganisms of Allobaculum and Oscillospira, while reducing those harmful ones like Sutterella at the genus level.DiscussionThese results suggested that LPN-1 supplementation may improve autism-like behaviors, possibly via regulating the gut microbiota.
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