This study aimed to investigate the effects of radiation (RT) on protein and protein S-palmitoylation levels in esophageal cancer (EC) cell lines. EC cells (N = 6) were randomly divided into RT and negative control. The results revealed that 592 proteins were identified in the RT group, including 326 upregulation proteins and 266 downregulation proteins. These differentially expressed proteins were involved in cellular biological processes. S-palmitoylation sequencing analysis revealed that 830 and 899 S-palmitoylation cysteine sites were upregulated and downregulated, respectively. Differential S-palmitoylation proteins were primarily found in cellular processes, anatomical entities, and binding activities. Kyoto encyclopedia of genes and genomes (KEGG) pathway and protein-protein interaction analysis revealed that differential S-palmitoylation proteins are involved in proteoglycans in cancer, shigellosis, EGFR tyrosine kinase inhibitor resistance, nucleocytoplasmic transport, and mineral absorption. In conclusion, this study demonstrated that RT significantly affects protein expression and S-palmitoylation levels in EC cell lines, which has implications for cancer biology-related cellular processes and pathways. These findings enhance understanding of the molecular mechanisms underlying the response of EC cells to RT treatment.

Plasma cell mastitis (PCM) is a non-bacterial inflammatory breast disorder affecting young and middle-aged nonpregnant and nonlactating women. However, a comprehensive and systematic analysis of PCM has not been conducted. Comprehensive cellular indexing of transcriptomes and epitopes by sequencing (CITE-seq) analysis was performed on 10,185 cells derived from PCM tissue to generate a highly detailed transcriptomic atlas. Thirteen distinct clusters were identified, and eight cell types were successfully annotated, including endothelial cells, common myeloid progenitor cells and neutrophils. Additionally, the overall alterations in immune cell composition in PCM patients were evaluated. Furthermore, differentially expressed genes between normal and PCM samples were assessed, and functional enrichment analysis was conducted. Finally, cellular communication and interaction were analysed to determine cell-to-cell communications. This study significantly contributes to the field of PCM, presenting a systematic and valuable perspective that serves as a fundamental resource for further exploration of the cellular and molecular mechanisms, pathogenesis of associated diseases and potential interventions.

Background. Radiation therapy is an effective local therapy for lung cancer. However, the interaction between genes and radiotherapy is multifaceted and intricate. Therefore, we explored the role of miR‐93‐5p in the proliferation, apoptosis, and migration abilities of A549 cells. Simultaneously, we also investigated the interactions between miR‐93‐5p and ionizing radiation (IR). Methods. Cell Counting Kit‐8, transwell, and apoptotic assay were performed to measure the proliferation, migration, and apoptosis abilities. The expression levels of miR‐93‐5p and its target gene in lung cancer were predicted using starBase v3.0. Then, data were validated using qPCR and western blot. Results. miR‐93‐5p significantly promoted the proliferation (P < 0.01) and migration abilities (P < 0.001) of A549 cells. Gasdermin E (GSDME) was identified to be a putative target of miR‐93‐5p and had a negative correlation with miR‐93‐5p (P < 0.001). Overexpression of miR‐93‐5p significantly decreased GSDME in A549 (P < 0.001). Interestingly, miR‐93‐5p decreased cell proliferation (P < 0.01) and cell migration (P < 0.01) and increased apoptosis (P < 0.01) in A549 cells after exposure to IR. Conclusions. miR‐93‐5p is presumed to play an oncogenic role in lung cancer by enhancing A549 cell proliferation and migration. It can enhance the sensitivity of radiotherapy under IR conditions. We speculate that the miR‐93‐5p/GSDME pathway was inhibited, activating the GSDME‐related pyroptosis pathway when the cells were exposed to IR. Therefore, miR‐93‐5p can overcome resistance to radiotherapy and improve the efficacy of radiotherapy.

Background: Exosomes are membrane‐bound vesicles with a diameter of 30–200 nm, and the microRNAs (miRNAs) they carry play important roles in cancer development. This study was aimed at investigating the expression and function of exosomal miRNAs in esophageal squamous cell carcinoma (ESCC). Methods: Exosomes were isolated from the plasma of ESCC patients via ultracentrifugation, followed by miRNA sequencing. GO, KEGG, and DO analyses were used to predict potential functions. Engineered exosomes were employed to deliver miR‐423‐5p mimics to ESCC cells, and CCK8, wound healing, transwell, and flow cytometry assays were conducted to evaluate cell proliferation, migration, invasion, and apoptosis. Results: Sequencing identified 182 miRNAs, with let‐7b‐5p and miR‐423‐5p being differentially expressed in exosomes from ESCC patients. Functional analysis indicated that these miRNAs may be involved in pathways such as axon guidance and the regulation of stem cell pluripotency. qRT‐PCR validation showed that miR‐423‐5p was downregulated in exosomes from ESCC patients but upregulated in cell lines. Overexpression of miR‐423‐5p suppressed tumor proliferation, migration, and invasion. It is worth noting that the low expression of miR‐423‐5p in ESCC tissues may be related to the increase in exosomal miR‐423‐5p in the local microenvironment, suggesting that tumor cells may export miR‐423‐5p via exosomes to maintain a malignant phenotype. Conclusion: Exosomal miR‐423‐5p and let‐7b‐5p play significant roles in the tumor microenvironment of ESCC, and exosome‐mediated delivery of miR‐423‐5p may represent a potential therapeutic strategy.