tsRNA modifications: An emerging layer of biological regulation in disease.

Background: Transfer RNA (tRNA)-derived small RNA (tsRNA) represents an important and increasingly valued type of small non-coding RNA (sncRNA). The investigation of tRNA and tsRNA modification crosswalks has not only provided novel insights into the information and functions of tsRNA, but has also expanded the diversity and complexity of the tsRNA biological regulation network.

Aim Of Review: Comparing with other sncRNAs, tsRNA biogenesis show obvious correlation with RNA modifications from mature tRNA and harbor various tRNA modifications.

Circular RNA LMBR1 inhibits bladder cancer progression by enhancing expression of the protein ALDH1A3.

Background: Circular RNAs (circRNAs) have been identified as playing an integral role in the development of bladder cancer (BC). However, the mechanism by which circRNAs operate in the chemical carcinogenesis of BC remains unclear.

Methods: To explore this mechanism, we used RNA high-throughput sequencing to identify differentially expressed circRNA in bladder epithelial cells and chemically induced malignant transformed BC cells.

A Novel tsRNA, mG-3' tiRNA Lys, Promotes Bladder Cancer Malignancy Via Regulating ANXA2 Phosphorylation.

Emerging evidence indicates that transfer RNA (tRNA)-derived small RNAs (tsRNAs), originated from tRNA with high abundance RNA modifications, play an important role in many complex physiological and pathological processes. However, the biological functions and regulatory mechanisms of modified tsRNAs in cancer remain poorly understood. Here, it is screened for and confirmed the presence of a novel mG-modified tsRNA, mG-3'-tiRNA Lys (mtiRL), in a variety of chemical carcinogenesis models by combining small RNA sequencing with an mG small RNA-modified chip.

Enhancing mA modification of lncRNA through METTL3 and RBM15 to promote malignant progression in bladder cancer.

Objective: Bladder cancer is one of the most prominent malignancies affecting the urinary tract, characterized by a poor prognosis. Our previous research has underscored the pivotal role of mA methylation in the progression of bladder cancer. Nevertheless, the precise relationship between N6-methyladenosine (mA) regulation of long non-coding RNA (lncRNA) and bladder cancer remains elusive.

mA modification mediates SLC3A2/SLC7A5 translation in 3-methylcholanthrene-induced uroepithelial transformation.

3-Methylcholanthracene (3-MC) is one of the most carcinogenic polycyclic aromatic hydrocarbons (PAHs). Long-term exposure to PAHs has been thought of as an important factor in urothelial tumorigenesis. N-methyladenosine (mA) exists widely in eukaryotic organisms and regulates the expression level of specific genes by regulating mRNA stability, translation efficiency, and nuclear export efficiency.

Effects of food-derived oligopeptide iron chelates on liver injury and gut microbiota homeostasis in iron-deficiency anemia female rats: a pilot study.

Iron deficiency (ID) is the biggest cause of anemia. This pilot study aimed to investigate the effects of food-derived oligopeptide iron chelates on ameliorating liver injury and restoring gut microbiota homeostasis in iron-deficiency anemia (IDA) female rats. Female Sprague-Dawley rats at 21 days old were selected and randomly divided into a control group ( = 4) and an ID model group ( = 16).

TROP2 translation mediated by dual mA/mG RNA modifications promotes bladder cancer development.

RNA modifications, including adenine methylation (mA) of mRNA and guanine methylation (mG) of tRNA, are crucial for the biological function of RNA. However, the mechanism underlying the translation of specific genes synergistically mediated by dual mA/mG RNA modifications in bladder cancer (BCa) remains unclear. We demonstrated that mA methyltransferase METTL3-mediated programmable mA modification of oncogene trophoblast cell surface protein 2 (TROP2) mRNA promoted its translation during malignant transformation of bladder epithelial cells.

Targeted mA demethylation of ITGA6 mRNA by a multisite dCasRx-mA editor inhibits bladder cancer development.

Introduction: N6-methyladenosine (mA) modification contributes to the pathogenesis and development of various cancers, including bladder cancer (BCa). In particular, integrin α6 (ITGA6) promotes BCa progression by cooperatively regulating multisite mA modification. However, the therapeutic effect of targeting ITGA6 multisite mA modifications in BCa remains unknown.

N-methyladenosine mediates Nrf2 protein expression involved in PM2.5-induced pulmonary fibrosis.

It has been reported that particulate matter with an aerodynamic diameter of <2.5 µm (PM2.5) could induce epithelial-mesenchymal transition (EMT)- and extracellular matrix (ECM)-related pulmonary fibrosis (PF).

NXPH4 Used as a New Prognostic and Immunotherapeutic Marker for Muscle-Invasive Bladder Cancer.

Background: One of the most common malignant tumors of the urinary system is muscle-invasive bladder cancer (MIBC). With the increased use of immunotherapy, its importance in the field of cancer is becoming abundantly evident. This study classifies MIBC according to GSVA score from the perspective of the GSEA immune gene set.

Food-derived bioactive oligopeptide iron complexes ameliorate iron deficiency anemia and offspring development in pregnant rats.

This study aimed to investigate anemia treatment and other potential effects of two food-derived bioactive oligopeptide iron complexes on pregnant rats with iron deficiency anemia (IDA) and their offspring. Rats with IDA were established with a low iron diet and then mated. There were one control group and seven randomly assigned groups of pregnant rats with IDA: Control group [Control, 40 ppm ferrous sulfate (FeSO)]; IDA model group (ID, 4 ppm FeSO), three high-iron groups (H-FeSO, 400 ppm FeSO; MCOP-Fe, 400 ppm marine fish oligopeptide iron complex; WCOP-Fe, 400 ppm whey protein oligopeptide iron complex) and three low-iron groups (L-FeSO, 40 ppm FeSO; MOP-Fe, 40 ppm marine fish oligopeptide iron complex; WOP-Fe, 40 ppm whey protein oligopeptide iron complex).

Global burden and inequality of iron deficiency: findings from the Global Burden of Disease datasets 1990-2017.

Background: Iron deficiency (ID) impairs patient physical activity, recognition and life quality, which is difficult to perceive but should not be underestimated. Worldwide efforts have been made to lower ID burden, however, whether it decreased equally in different regions and sexes is unclear. This study is to examine regional and sex inequalities in global ID from 1990 to 2017.

Alteration in glycolytic/cholesterogenic gene expression is associated with bladder cancer prognosis and immune cell infiltration.

Background: Oncogenic metabolic reprogramming contributes to tumor growth and immune evasion. The intertumoral metabolic heterogeneity and interaction of distinct metabolic pathways may determine patient outcomes. In this study, we aim to determine the clinical and immunological significance of metabolic subtypes according to the expression levels of genes related to glycolysis and cholesterol-synthesis in bladder cancer (BCa).

METTL1-m G-EGFR/EFEMP1 axis promotes the bladder cancer development.

Background: The posttranscriptional modifications of transfer RNA (tRNA) are critical for all aspects of the tRNA function and have been implicated in the tumourigenesis and progression of many human cancers. By contrast, the biological functions of methyltransferase-like 1 (METTL1)-regulated m G tRNA modification in bladder cancer (BC) remain obscure.

Results: In this research, we show that METTL1 was highly expressed in BC, and its level was correlated with poor patient prognosis.

N6-Methylandenosine-Related lncRNAs Predict Prognosis and Immunotherapy Response in Bladder Cancer.

Both lncRNAs and the N6-methyladenosine (m6A) modification are key regulators of tumorigenesis and innate immunity. However, little is known about the m6A modification of lncRNAs and their clinical and immune relevance in bladder cancer. In this study, we identified m6A-related lncRNAs using Pearson correlation analysis in The Cancer Genome Atlas (TCGA) and the IMvigor210 datasets.

Integrated analysis of mRNA-mA-protein profiles reveals novel insights into the mechanisms for cadmium-induced urothelial transformation.

This study aimed to investigate the mechanisms underlying Cd-induced urothelial transformation, using multi-omics analyses (transcriptome, epitranscriptome, and proteome). Transcriptomics analysis was performed to estimate the expression of genes, methylated RNA immunoprecipitation sequencing analysis was used to detect mA modification, while proteomics analysis was used to identify differentially expressed proteins. Differentially expressed genes (DEGs) were subjected to Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analysis.

Programmable N6-methyladenosine modification of CDCP1 mRNA by RCas9-methyltransferase like 3 conjugates promotes bladder cancer development.

Accumulating evidence has revealed significant roles for N6-methyladenosine (m 6 A) modification in the development of various cancers. We previously demonstrated an oncogenic role of m 6 A-modified CUB domain containing protein 1 (CDCP1) in bladder cancer (BC) progression. However, the biological functions and underlying molecular mechanisms of engineered programmable m 6 A modification of CDCP1 mRNA in BC remain obscure.

N-methyladenosine modification of ITGA6 mRNA promotes the development and progression of bladder cancer.

Background: Accumulating evidence has revealed the critical roles of N-methyladenosine (mA) modification of mRNA in various cancers. However, the biological function and regulation of mA in bladder cancer (BC) are not yet fully understood.

Methods: We performed cell phenotype analysis and established in vivo mouse xenograft models to assess the effects of mA-modified ITGA6 on BC growth and progression.

Salmonella enterica Serovar Typhimurium Interacts with CD209 Receptors To Promote Host Dissemination and Infection.

serovar Typhimurium, a Gram-negative bacterium, can cause infectious diseases ranging from gastroenteritis to systemic dissemination and infection. However, the molecular mechanisms underlying this bacterial dissemination have yet to be elucidated. A study indicated that using the lipopolysaccharide (LPS) core as a ligand, Typhimurium was able to bind human dendritic cell-specific intercellular adhesion molecule-3-grabbing nonintegrin (hCD209a), an HIV receptor that promotes viral dissemination by hijacking antigen-presenting cells (APCs).

Dynamic mA mRNA methylation reveals the role of METTL3-mA-CDCP1 signaling axis in chemical carcinogenesis.

N6-methyladenosine (mA) is the most abundant internal modification in mammalian mRNAs. Despite its functional importance in various physiological events, the role of mA in chemical carcinogenesis remains largely unknown. Here we profiled the dynamic mA mRNA modification during cellular transformation induced by chemical carcinogens and identified a subset of cell transformation-related, concordantly modulated mA sites.

Exploits CD209 Receptors for Promoting Host Dissemination and Infection.

is a Gram-negative enteropathogen and causes gastrointestinal infections. It disseminates from gut to mesenteric lymph nodes (MLNs), spleen, and liver of infected humans and animals. Although the molecular mechanisms for dissemination and infection are unclear, many Gram-negative enteropathogens presumably invade the small intestine via Peyer's patches to initiate dissemination.

Characterization of the enterovirus 71 P1 polyprotein expressed in Pichia pastor as a candidate vaccine.

Human enterovirus 71 (EV71) plays an important role in hand, foot, and mouth disease (HFMD), which recently caused the death of hundreds of children in the Asia-Pacific region. However, there are no specific treatments available for EV71 infections; thus, a safe and effective vaccine is needed urgently. In this study, we developed an effective and economical method for producing EV71 polyprotein (P1 protein) in Pichia pastoris.