The gut microbiota plays important roles in chronic inflammation and colon cancer. Lactobacillus is a gut-resident probiotic with benefits to host health. We recently identified Lactobacillus plantarum strain YYC-3 with strong inhibition against two colon cancer cell lines (HT-29 and Caco2). However, the inhibitory effect of YYC-3 against colon cancer in vivo has not been verified. Thus, in the present study, we explored the probiotic function of strain YYC-3 and its cell-free supernatant (YYCS) respectively in the APCMin/+ mouse model of colon cancer during tumour development and growth, and the underlying anti-cancer mechanism. Treatment of both strain YYC-3 and the YYCS prevented the occurrence of colon tumours and mucosal damage in APCMin/+ mice fed a high-fat diet, although YYC-3 had a stronger anti-cancer effect. The mechanism involved modulation of the immune system and downregulated expression of the inflammatory cytokines interleukin (IL)-6, IL-17 F, and IL-22, along with reduced infiltration of inflammatory cells. Moreover, YYC-3 suppressed activation of the NF-κB and Wnt signalling pathways, and restored the altered gut microbiota composition to closely match that of wild-type mice. These results lay a theoretical foundation for application of YYC-3 in colon cancer prevention.

RBM15 expression is recurrently upregulated in several types of malignant tissues, and its high expression level is typically associated with poor prognosis. However, whether and how RBM15 is involved in the tumor progression remains unclear. In this study, we found that overexpressing RBM15 in NIH3T3 cells was able to enhance proliferation rate in vitro and induced subcutaneous tumor formation in vivo . Moreover, we imaged the subcellular localization of RBM15 with our home-built structured illumination super-resolution microscopy, and revealed that RBM15 formed substantial condensates dispersed in the nucleus, undergoing dynamic fusion and fission activities. These condensates were partially colocalized with m ⁶ A-modified transcripts in the nucleus. In addition, we confirmed that RBM15 formed “liquid-like” droplets in a protein/salt concentration-dependent manner in vitro , and the addition of RNA further enhanced its phase-separation propensity. To identify downstream targets of RBM15, we performed meRIP-seq and RNA-seq, revealing that RBM15 preferentially bound to and promoted the m ⁶ A modification on the mRNA of Serine/threonine/tyrosine kinase 1 (STYK1), thereby enhancing its stability. The upregulated STYK1 expression caused MAPK hyperactivation, thereby leading to oncogenic transformation of NIH3T3 cells.

Background: Spinal ependymal tumors are a diverse group of neoplasms encompassing four subtypes: spinal ependymoma (SP-EPN), spinal ependymoma, MYCN -amplification (SP-EPN- MYCN ), spinal myxopapillary ependymoma (SP-MPE), and spinal subependymoma (SP-SE). However, the molecular differences among these subtypes remain largely unknown. Methods: Using an integrated multi-omics approach (whole-genome sequencing, RNA-seq, and mass spectrometry), we identified the distinct molecular characteristics of three subtypes except for SP-EPN- MYCN . Results: In SP-EPN, abnormal enrichment of ciliary signaling, particularly involving the MKS complex, was evident. SP-MPE exhibited significant dysregulation of mitochondrial metabolism, reflecting a metabolic profile aligned with the Warburg effect. SP-SE tumors showed enhanced activity of immune-related pathways, including interferon signaling and extracellular vesicle dynamics, suggesting a distinct tumor microenvironment. Conclusion: This pilot study identifies candidate molecular markers in a single-center spinal ependymal tumor cohort. Clinical trial number: Not applicable.