Bacterial translocation is a pathological process involving migration of pathogenic bacteria across the intestinal barrier to enter the systemic circulation and gain access to distant organs. This phenomenon has been linked to a diverse range of diseases including inflammatory bowel disease, pancreatitis, and cancer. The intestinal barrier is an innate structure that maintains intestinal homeostasis. Pathogenic infections and dysbiosis can disrupt the integrity of the intestinal barrier, increasing its permeability, and thereby facilitating pathogen translocation. As translocation represents an essential step in pathogenesis, a clear understanding of how barrier integrity is disrupted and how this disruption facilitates bacterial translocation could identify new routes to effective prophylaxis and therapy. In this comprehensive review, we provide an in-depth analysis of bacterial translocation and intestinal barrier function. We discuss currently understood mechanisms of bacterial–enterocyte interactions, with a focus on tight junctions and endocytosis. We also discuss the emerging concept of bidirectional communication between the intestinal microbiota and other body systems. The intestinal tract has established ‘axes’ with various organs. Among our regulatory systems, the nervous, immune, and endocrine systems have been shown to play pivotal roles in barrier regulation. A mechanistic understanding of intestinal barrier regulation is crucial for the development of personalized management strategies for patients with bacterial translocation-related disorders. Advancing our knowledge of barrier regulation will pave the way for future research in this field and novel clinical intervention strategies.

Background: SLC30 family genes, also known as ZnT family genes, can keep cellular zinc levels within a physiological range by exporting zinc to extracellular space or by isolating zinc in the specific regions of cytoplasm when cellular zinc concentrations are elevated in human cells. There are growing evidences that dysregulated expression of SLC30 family genes can potentially influence tumorigenesis. However, the expression and prognostic value of SLC30 family genes in cervical carcinoma are poorly characterized. Methods: In this study, we used many tools such as UALCAN, Kaplan-Meier Plotter, cBioPortal, LinkedOmics, FunRich, Metascape, GeneMANIA, Open targets and TISIDB to perform bioinformatics analysis of SLC30 family genes in cervical carcinoma. Results: We found that the expression of SLC30A1/7/10 was significantly higher in cervical carcinoma than that in normal matched tissues, while SLC30A2/8 mRNA levels were decreased compared to normal tissues. For tumor stages, SLC30A1, SLC30A7 and SLC30A10 groups significantly varied. And a high expression of SLC30A1, SLC30A6, SLC30A8 and SLC30A10 was associated with worse overall survival in cervical carcinoma patients. Besides, we found that SLC30A1/10 may have a potential regulatory role in immune infiltration in cervical carcinoma. In addition, the results showed that the high expression of SLC30A1 was resistant to 79 drugs or small molecules; Two drugs (Neopeltolide and Tozasertib) can inhibit the high expression of SLC30A10 in cancers. Conclusion: SLC30A1 and SLC30A10 can be recognized as potential diagnostic indicators and therapeutic targets in cervical carcinoma.

Background RGMB antisense RNA 1 ( RGMB-AS1 ) is a member of long non-coding RNAs (lncRNAs) and relates to the carcinogenesis of numerous cancers. Nonetheless, its performance and mechanism in cervical cancer (CC) is unclear. Methods The expressions of RGMB-AS1 , microRNA-4428 ( miR-4428 ), PBX homeobox 1 ( PBX1 ) were analyzed by quantitative real-time PCR (qRT-PCR). Nuclear-cytoplasmic fractionation was used to locate RGMB-AS1 . Cell counting kit-8 (CCK-8), EdU, TUNEL, Western blot and transwell assays were performed to assess RGMB-AS1 function in proliferation, apoptosis, and invasion in vitro . Interplays involving miR-4428 , RGMB-AS1 and PBX1 were verified applying luciferase reporter, RNA pull-down and RNA immunoprecipitation (RIP). Results RGMB-AS1 level was high in CC specimens and cells. RGMB-AS1 encouraged proliferation, and invasion, and depressed apoptosis in CC cells. Further, miR-4428 was screened as a targeted for RGMB-AS1 , and RGMB-AS1 performed the competitive endogenous RNA (ceRNA) role to release PBX1 from miR-4428. Correlation analysis based on clinical specimens confirmed positive association between RGMB-AS1 and PBX1 and negative association of miR-4428 with RGMB-AS1 and PBX1 . Rescue experiments indicated that PBX1 overexpression counteracted RGMB-AS1 silence-caused inhibition on CC development. Conclusions RGMB-AS1 regulated miR-4428 / PBX1 axis to aggravate CC development, indicating that targeting RGMB-AS1 could be a potent way for developing the novel therapeutic methods for CC patients.