Colorectal cancer (CRC) remains a significant global health challenge, characterized by high morbidity and mortality. Despite advances in surgical techniques, chemotherapy, targeted therapies, and immunotherapy, many CRC cases exhibit treatment resistance and immune evasion, necessitating the identification of novel therapeutic targets. Follistatin-like protein 3 (FSTL3) has recently emerged as a key regulator in CRC progression, influencing immune suppression and therapy resistance. FSTL3 modulates the tumor microenvironment by promoting epithelial-mesenchymal transition (EMT), sustaining β-catenin signaling, and stabilizing c-Myc, which collectively enhance tumor invasiveness and metastatic potential. Additionally, FSTL3 contributes to immune evasion by upregulating immune checkpoint molecules such as programmed death-ligand 1  (PD-L1) and indoleamine-2,3-dioxygenase 1 (IDO1), thereby suppressing cytotoxic T-cell activity. High FSTL3 expression correlates with poor prognosis and resistance to conventional chemotherapy, targeted agents, and immune checkpoint inhibitors. Given its pivotal role in CRC pathophysiology, FSTL3 represents a promising biomarker for disease prognosis and a potential therapeutic target. Future research should focus on developing FSTL3-targeted interventions, including monoclonal antibodies, small-molecule inhibitors, and combination strategies with immunotherapy. Understanding the precise molecular mechanisms underlying FSTL3-mediated tumor progression and immune escape will be essential for translating these insights into clinical applications.

This study explored the mechanisms of action of inflammation related central genes in severe depression (MDD) and analyzes their potential as therapeutic targets. By identifying key genes and establishing the link between immune regulatory mechanisms and depression, we provide a theoretical basis for developing more accurate diagnostic and treatment methods.
Gene expression datasets related to MDD were obtained from the Gene Expression Omnibus (GEO). Differentially expressed genes (DEGs) associated with inflammatory processes were identified and analyzed through Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. Protein-protein interaction (PPI) networks were constructed to identify hub genes. Additionally, we explored regulatory networks of miRNAs, transcription factors, and potential drug interactions were explored. Immune infiltration analysis was performed to examine immune cell profiles.
Seven key genes—HMGB1, HSP90AB1, MAPK1, MMP9, MYD88, S100A12, and TLR2—were identified as central players in the inflammatory pathways underlying MDD. These genes demonstrated moderate diagnostic accuracy with AUC values ranging from 0.5 to 0.7. Enrichment analyses revealed significant associations with immune signaling pathways, including IL-17 and Toll-like receptor signaling. Immune infiltration analysis highlighted altered abundances of regulatory T cells, neutrophils, and dendritic cells in MDD samples.
Inflammatory-related hub genes play crucial roles in linking immune dysregulation to the pathophysiology MDD pathophysiology. These findings offer insights into the immunological underpinnings of MDD and present potential therapeutic targets for intervention through immune-modulatory approaches.

Colorectal cancer (CRC) is a leading cause of cancer-related mortality, with high-risk cases showing increased aggressiveness and poor prognosis. Recent studies suggest that long noncoding RNAs (lncRNAs) such as C6orf223 may play crucial roles in CRC progression. This study investigated the expression and regulatory role of C6orf223 in high-risk versus low-risk CRC patients, focusing on its potential as a biomarker for diagnosis and prognosis.
We conducted differential expression analysis using RNA-seq data to identify key genes in high-risk CRC, followed by correlation and pathway enrichment analyses to understand C6orf223. Kaplan-Meier survival analysis and receiver operating characteristic (ROC) curves assessed the prognostic and diagnostic potential of C6orf223. RNA methylation and mutation patterns were analyzed to explore post-transcriptional regulation and genetic alterations in high-risk CRC.
C6orf223 was significantly upregulated in high-risk CRC. High C6orf223 expression was associated with poor overall survival, and a biomarker panel that includes C6orf223 and microRNAs showed strong potential for accurate diagnosis. Methylation and mutation analyses revealed potential mechanisms enhancing C6orf223’s stability and oncogenic activity.
Our findings indicate that C6orf223 acts as a binder to and inhibits tumor-suppressive microRNAs, reducing their availability to regulate cancer-promoting genes and may serve as a valuable biomarker for CRC diagnosis and prognosis. Further research on lncRNA-microRNA interactions could provide insights for novel CRC therapies.

It can sometimes be very difficult to control the manifestations of autoimmunity and lymphoproliferation in patients with primary immunodeficiency diseases, and there is no adequate response to first-line treatments. Rituximab (RTX), as a second-line treatment, is efficacious and well-tolerated for the management of these clinical manifestations.
This retrospective study was conducted to analyze the clinical, immunological, and genetic findings together with the response rate to RTX therapy in subjects with inborn errors of immunity (IEI) and autoimmune or autoinflammatory manifestations. In this study, 23 individuals with IEI and autoimmune or lymphoproliferation manifestations who received RTX between April 2008 and 2021 were evaluated.
Fifteen out of the 23 patients were female. The median age of cases was 12 years.  The moderate and severe adverse reactions, including fever, diarrhea, and anaphylaxis shock, were manifested during RTX infusion in 5 patients. In total, 86.9% of patients responded to rituximab (complete response: n=14, partial response: n=6) while three failed to respond. The median response time to RTX treatment was 50 days. All patients were given monthly intravenous immunoglobulin (IVIG) therapy. Pneumonia and candidiasis occurred in one patient a week after receiving the second injection of RTX. Eight patients expired during follow-up.
In conclusion, the response rate of RTX could be improved through administering monthly IVIG for hypogammaglobulinemia treatment following RTX infusion. Early use of rituximab leads to a better response rate in comparison with late use of rituximab in multitreated refractory patients. The efficient cumulative dose of rituximab remains undefined. 

The impacts of the CXC motif chemokine 12 (CXCL12)/ C-X-C chemokine receptor type 4 (CXCR4) axis on the infiltration of anti-tumor and pro-tumor immune cells in the tumor microenvironment (TME) of breast cancer (BCa) have been noted in previous studies. Accordingly, regulating the downstream signals of this axis can effectively increase CD8⁺ cytotoxic T cells and decrease the frequency of immunosuppressive cells in the TME. This study investigated the anti-tumor effects of N, N''-thiocarbonylbis (N'-(3,4-dimethylphenyl)-2,2,2 trifluoroacetimidamide) (A1), a novel fluorinated CXCR4 inhibitor on a BCa cell line.
In this study, the impacts of A1 on cell viability, proliferation, apoptosis, and cell cycle were examined using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and flow cytometry assays. Moreover, the effect of A1 on the number of CXCR4⁺ 4T1 cells was measured by flow cytometry.
A1 treatment exhibited cytotoxic effects on 4T1 cells, promoting cell apoptosis and G₂/M cell cycle arrest. In addition, A1-treated cells showed a reduced cell proliferation than CXCL12 treated cells. Furthermore, treatment with A1 alongside CXCL12 significantly decreased the number of CXCR4⁺ cells compared to the control group treated with only CXCL12 as a proliferator factor.
These results indicate that A1 exerts potential anti-tumor effects and may serve as a possible therapeutic agent for BCa treatment; however, further studies are required.

Cervical cancer is a significant public health concern, particularly in women infected with the human papillomavirus (HPV). Recent evidence suggests that host genetic factors, specifically those related to the human leukocyte antigen (HLA) system, may also play a crucial role in determining susceptibility to cervical cancer in HPV-infected individuals.
In this study, 86 patients with HPV and 27 healthy donors were selected from May 2023 to February 2024. HLA-DRB1 genotypes were determined using polymerase chain reaction followed by high-resolution melting curve analysis (HRM). Genotype frequencies in patients were compared with those in the control group from donors.
Based on the HRM analysis, 10 genotypes were found in both patients and controls (profiles A-J). In the analysis of HLA-DRB1 genotypes, C, F, and I showed significant associations with HPV infection, indicating a possible protective effect against infection. Notably, genotype B was strongly linked to high-risk HPV, while genotype A was associated with low-risk HPV and is relevant to infection history. However, the remaining genotypes examined in the study did not exhibit significant associations with the analyzed parameters.
This study contributes valuable evidence regarding the role of HLA-DRB1 genotypes in cervical cancer susceptibility and highlights the potential clinical implications for risk assessment and targeted immunotherapies. The use of HRM for HLA typing offers advantages that are efficient, accurate, and scalable, making it suitable for large-scale studies and clinical applications.

Spinal cord injuries (SCI) lead to complex primary and secondary damage that disrupts neural function. Current treatments are often insufficient and unable to fully repair spinal cord injuries, highlighting the urgent need for new medicines and innovative therapies.
This study aimed to evaluate the therapeutic potential of abscisic acid (ABA) in SCI by examining its effects on immune-inflammatory genes’ expression in rats. This phytohormone possesses anti-inflammatory and neuroprotective properties, rendering it a potential agent for reducing secondary damage following spinal cord injury. Additionally, we performed protein-protein interaction (PPI), pathway enrichment, functional annotation, and gene ontology (GO) analyses to gain a comprehensive understanding of the functions of the affected genes.
Based on the results, SCI led to changes in the expression of immune/inflammation-related genes in rats. However, the administration of ABA alleviated the effects. ABA downregulated proinflammatory genes (IL-6, IL-1β, MCP, TLR2, TLR4) and neural signaling components (NMDA, AMPA, NK1R), while upregulating adrenergic receptors (ADRA1A, ADRB1) and a gamma-aminobutyric acid receptor (AGBRA2). PPI analysis identified FOS, IL-1β, IL-6, MMP9, and TLR4 as crucial nodes in the network, exhibiting the highest degree of interaction. Functional analyses revealed potential impacts on cellular responses, metabolic processes, and synapse-associated extracellular matrix components. Notably, these genes were enriched in inflammatory signaling pathways according to KEGG analysis.
These findings suggest that ABA has a significant modulatory effect on gene expression following SCI, particularly in reducing inflammation and immune responses, thereby highlighting its potential as a novel therapeutic agent for SCI.

To explore the relationship between thioredoxins (Trx) -2, systemic-immune inflammatory index (SII), and short-term major adverse cardiac events (MACE) in septic cardiomyopathy (SCM).
A retrospective study was conducted on 98 SCM patients admitted to Affiliated Jinling Hospital, Medical School of Nanjing University Emergency Intensive Care Unit (EICU) from July 2022 to June 2024. Patients underwent routine blood tests and data assessment upon admission. Based on the occurrence of MACE by day 28, patients were divided into the MACE group and the non-MACE (N-MACE) group. Clinical data were collected, and logistic regression, along with restricted cubic spline models, analyzed the relationships between SII, Trx-2, and MACE risk in SCM patients.
Among the 98 SCM patients included, there were 35 (35.71%) in the MACE group and 63 (64.29%) in the N-MACE group. Logistic regression analysis showed that elevated SII and serum Trx-2 levels correlated with an increased risk of MACE within 28 days post-admission for SCM patients. Restricted cubic spline analysis revealed a linear dose-response relationship between both SII and Trx-2 levels with short-term MACE risk in SCM. The ROC curve showed AUC values of 0.869 for LVEF, 0.881 for SII, while combining SII + Trx-2 yielded 0.926 (95% CI: 0.862-0.989), with specificity at 83.98 % and sensitivity at 98.80%.
The abnormal increase of serum SII and Trx-2 levels in SCM patients is related to the occurrence of MACE within 28 days after admission. The risk of MACE increases with the increase of serum SII and Trx-2 levels.

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