Background: Tripartite Motif 29 (TRIM29) has been newly identified as being implicated in cancer progression. However, the biological role and molecular mechanism of TRIM29 in the invasion and metastasis of colorectal cancer (CRC) remain to be determined. Methods: The expression levels of TRIM29 and β-catenin in CRC patient specimens were detected by immunohistochemistry. Recombinant lentivirus vectors containing the TRIM29 gene and its small hairpin interfering RNAs were constructed and transduced into CRC cells. Wound-healing and Transwell assays were performed to evaluate the migration and invasion abilities of CRC cells in vitro. Hepatic metastasis models in nude mice were established to validate the function of TRIM29 in vivo. Moreover, the expressions of epithelial-to-mesenchymal transition (EMT)-associated proteins were detected by qRT-PCR and Western blotting in CRC cells. Finally, Western blotting, qRT-PCR, luciferase reporter assays, and immunofluorescence assays were used to explore the molecular mechanisms of TRIM29 in CRC progression. Results: Increased TRIM29 expression positively correlated with lymph node metastasis and β-catenin expression in patient CRC tissues. Overexpression of TRIM29 promoted invasion and metastasis of CRC cells in vitro and in vivo by regulating EMT, whereas the knockdown of TRIM29 had the opposite effect. Further mechanistic studies suggest that TRIM29 can activate the Wnt/β-catenin signaling pathway via up-regulating CD44 expression in colorectal cancer. Conclusions: TRIM29 induces EMT through activating the Wnt/β-catenin signaling pathway via up-regulating CD44 expression, thus promoting invasion and metastasis of CRC.

Over the past decade, the large-scale spread of influenza viruses has posed an increasing burden on public health. The effective screening of influenza agents requires a fast, precise, on-site and easy-to-operate method. Unfortunately, current screening methods face challenges in speed and accuracy, especially in complex on-site settings. Here, this work develops a nucleoprotein antibody-modified graphene field-effect transistor (NPAb-GFET) for rapid and highly precise detection of influenza A viruses. The functionalized monoclonal antibodies capture influenza virus nucleoprotein within 100 × 10⁻⁹ s on the sensing surface. Therefore, the developed NPAb-GFET achieves an average response time of 72.1 s when detecting influenza A viruses in clinical samples. Furthermore, the testing of 106 throat swab samples exhibits an accuracy of 99.1%. This finding provides a valuable diagnostic tool for the control of influenza viruses, accelerating the population-wide control of other epidemics.

Background: Consensus Molecular Subtype (CMS) 4 and BRAF mutations are poor prognostic indicators for colon adenocarcinoma (COAD). Although the prevalence of BRAF-mutated COAD is higher in the CMS1 subtype, we have identified certain cases of CMS4 subtypes in patients with BRAF mutations. However, there is currently a lack of research exploring whether this particular type of COAD exhibits a worse prognosis and unraveling its underlying mechanism. Methods: This retrospective study analyzed the transcriptome profiles and clinical parameters of COAD patients from six public datasets. Kaplan–Meier plots and bioinformatics methods predicted the correlation between ATP23 expression and patient survival. We compared enriched pathways, genomic mutations, immune cell infiltration, copy number alterations, cell–cell communication, and TIDE scores between ATP23-high and ATP23-low groups. Furthermore, in vitro experiments verified the potential roles of ATP23 in COAD. Results: The expression of ATP23 was significantly lower in tumor tissues, particularly in the CMS4 subtype. No significant correlation was observed between ATP23 expression and clinical characteristics or molecular mutations in COAD. Higher ATP23 levels were associated with improved survival rates in COAD patients. In vitro experiments indicated that ATP23 inhibits the proliferation, migration, and invasion capabilities of COAD cells. Moreover, decreased ATP23 expression may impair oxidative phosphorylation in T cells, contributing to the formation of an immune-evasive microenvironment, and potentially leading to reduced efficacy of both immunotherapy and conventional chemotherapy. Conclusions: ATP23 is a potential prognostic marker for COAD patients. Reduced ATP23 expression may inhibit oxidative phosphorylation in T cells and contribute to the formation of an immunosuppressive microenvironment.