Disulfidptosis, a newly discovered type of programmed cell death, could be a mechanism of cell death controlled by SLC7A11. This could be closely associated with tumor development and advancement. Nevertheless, the biological mechanism behind disulfidptosis-related genes (DRGs) in sarcoma (SARC) is uncertain. This study identified three valuable genes (SLC7A11, RPN1, GYS1) associated with disulfidptosis in sarcoma (SARC) and developed a prognostic model. The multiple databases and RT-qPCR data confirmed the upregulated expression of prognostic DRGs in SARC. The TCGA internal and ICGC external validation cohorts were utilized to validate the predictive model capacity. Our analysis of DRG riskscores revealed that the low-risk group exhibited a more favorable prognosis than the high-risk group. Furthermore, we observed a significant association between DRG riskscores and different clinical features, immune cell infiltration, immune therapeutic sensitivity, drug sensitivity, and RNA modification regulators. In addition, two external independent immunetherapy datasets and clinical tissue samples were collected, validating the value of the DRGs risk model in predicting immunotherapy response. Finally, the SLC7A11/hsa-miR-29c-3p/LINC00511, and RPN1/hsa-miR-143-3p/LINC00511 regulatory axes were constructed. This study provided DRG riskscore signatures to predict prognosis and response to immunotherapy in SARC, guiding personalized treatment decisions.

Background: N7-methylguanosine (m7G) methylation is an RNA modification associated with cancer progression, but its specific role in head and neck squamous cell carcinoma (HNSCC) remains unclear.Methods: This study analyzed the differential expression of m7G-related genes (m7GRGs) in HNSCC using the TCGA-HNSCC dataset, identifying key pathways associated with the cell cycle, DNA replication, and focal adhesion. A LASSO-Cox regression model was constructed based on four m7GRGs (EIF3D, EIF1, LARP1, and METTL1) and validated with GEO datasets and clinical samples. Further validation of gene upregulation in HNSCC tissues was conducted using RT-qPCR and immunohistochemistry, while the role of LARP1 in HNSCC cells was assessed via knockout experiments.Results: The constructed model demonstrated strong predictive performance, with the risk score significantly correlating with prognosis, immune infiltration, and drug sensitivity. An external dataset and clinical specimens further confirmed the model’s predictive accuracy for immunotherapy response. Additionally, two regulatory axes—LINC00707/hsa-miR-30b-5p/LARP1 and SNHG16/hsa-miR-30b-5p/LARP1—were identified. LARP1 knockout experiments revealed that suppressing LARP1 markedly inhibited HNSCC cell proliferation, migration, and invasion.Conclusion: The m7GRG-based prognostic model developed in this study holds strong clinical potential for predicting prognosis and therapeutic responses in HNSCC. The identification of LARP1 and its related regulatory pathways offers new avenues for targeted therapy in HNSCC.

Objective: The efficacy of concurrent chemoradiotherapy (CRT) after induction chemotherapy (IC) in the treatment of esophageal squamous cell carcinoma (ESCC) remains unclear. The purpose of this study was to explore the efficacy of IC in patients with ESCC.Methods: 124 patients with ESCC receiving CRT were included. Patients were divided into IC+CRT group and CRT group. Short-term and long-term efficacy as well as survival time of the two groups were compared, influencing factors of IC efficacy were investigated, and overall survival (OS) and progression-free survival (PFS) between the two groups were compared in different subgroups.Results: There was no significant difference in the objective response rate (ORR) between the two groups. After IC, the ORR was higher in patients with single-drug concurrent chemotherapy weekly and patients with effective IC. In the long-term efficacy, advanced clinical stage patients had a shorter PFS compared to early-stage patients, and chemoradiotherapy mode ameliorates patients’ PFS. OS and PFS of IC+CRT group were longer than that of CRT group in both tumor diameter <5cm and single-drug chemotherapy weekly subgroups. In addition, OS of IC+CRT group was longer than that of CRT group in pathological grade G1-2 subgroup.Conclusions: IC improve the efficacy and survival rate of patients with locally advanced ESCC, and the benefits are more advantageous in subgroups of effective IC, pathological grade G1-2, tumor diameter < 5cm, single-drug concurrent chemotherapy weekly.

Background: Glioma is a molecularly heterogeneous tumor of the central nervous system with variable clinical behavior, immune contexture, and therapeutic response. Palmitoylation is a reversible lipid modification that regulates membrane localization, synaptic signaling, inflammatory pathways, and oncogenic signaling; however, the prognostic and functional relevance of palmitoylation-related long non-coding RNAs (PRlncRNAs) in glioma remains incompletely defined. Methods: Transcriptomic and clinical data for 429 glioma patients were obtained from TCGA. Thirty palmitoylation-related genes were used to identify PRlncRNAs through co-expression analysis. A prognostic signature was constructed using univariate Cox regression, LASSO-Cox regression, and multivariate Cox regression. The model was evaluated by Kaplan-Meier analysis, ROC curves, time-dependent ROC analysis, Cox regression, C-index analysis, nomogram modeling, calibration curves, and an institutional clinical cohort of 46 paired glioma and adjacent tissues. Functional enrichment, immune deconvolution, tumor microenvironment scoring, TIDE-based immunotherapy prediction, TMB/MSI analysis, and pRRophetic-based drug-sensitivity analysis were performed. U87 and U251 glioma cells, LYRM4-AS1 knockdown, in vitro functional assays, and nude-mouse xenografts were used for biological validation. Results: A six-PRlncRNA signature consisting of POLR2J4, LYRM4-AS1, BX640514.2, AL592295.6, AL390755.1, and AC018730.1 stratified glioma patients into high- and low-risk groups with significantly different overall survival. The risk score remained an independent prognostic factor and showed strong predictive performance for 1-, 3-, and 5-year survival. Risk-associated genes were enriched in extracellular matrix organization, leukocyte-mediated immunity, neuroactive ligand-receptor interaction, MAPK signaling, cytokine-receptor interaction, cell-cycle programs, and ECM-receptor interaction. High-risk tumors displayed increased stromal, immune, and ESTIMATE scores, higher expression of multiple immune checkpoint genes, higher TIDE scores, and elevated TMB/MSI levels. Clinical validation confirmed differential expression of the six PRlncRNAs and the prognostic value of the risk score. Functionally, LYRM4-AS1 knockdown inhibited glioma cell proliferation, EdU incorporation, migration, invasion, and colony formation, while suppressing xenograft growth, increasing TUNEL-positive apoptotic cells, and reducing Ki-67, CD31, and MMP9 expression. Conclusion: This study identifies a palmitoylation-related lncRNA signature that integrates molecular signaling, immune remodeling, and prognosis in glioma. LYRM4-AS1 acts as a functional driver of glioma progression and may represent a candidate biomarker and therapeutic target at the crossroads of neural tumorigenesis and immune-microenvironmental regulation.

Background: N7-methylguanosine (m7G) methylation is a widespread modification in RNA, which is very important for various biological functions and is closely associated with the occurrence and development of cancer. However, the expression of m7G methylation-related genes (m7GRGs) in head and neck squamous cell carcinoma (HNSCC) and its correlation with prognosis remain unclear. Methods: In this study, the expression pattern and prognosis of m7GRGs in TCGA-HNSCC was discussed through a public database. The differentially expressed genes (DEGs) between high and low expression groups of m7GRGs were identified, and their functional enrichment was analyzed. The prognostic m7GRG expression in HNSCC was verified by real-time quantitative PCR(RT-qPCR). LASSO-Cox regression analysis was performed to construct a prognostic model and predictive nomogram. In addition, the relationship between the expression of prognostic m7GRGs in HNSCC and clinicopathological features, copy number variation (CNV), tumor microenvironment (TME), tumor mutation burden (TMB), microsatellite instability (MSI), ESTIMATE, mRNA stemness index (mRNAsi), and drug sensitivity was evaluated. Finally, the competitive endogenous RNA (ceRNA) regulatory network was constructed based on the expression level of prognostic m7GRGs. Results: m7GRGs were closely related to cell cycle, DNA replication and repair, and focal adhesion, among other factors. The gene mutation map of m7GRGs in HNSCC was summarized. Further, an HNSCC-related prognostic model including four prognostic biomarkers (EIF3D, EIF1, LARP1, and METTL1) was constructed. The verification of RT-qPCR data further confirmed the upregulated expression of prognostic m7GRGs in HNSCC. Prognostic m7GRGs were significantly correlated with tumor stage, grade, TMB, MSI, immune infiltration, mRNAsi, and drug sensitivity. Finally, the LINC00707/hsa-miR-30b-5p/LARP1 and SNHG16/hsa-miR-30b-5p/LARP1 regulatory axes of HNSCC were constructed. Conclusion: We found a significant correlation between the abnormal expression of m7GRGs and the prognosis of patients with HNSCC. We identified four m7GRGs prognostic models that can effectively evaluate the prognosis of patients with HNSCC, and these provide a basis for individualized treatment and immunotherapy decision-making in HNSCC patients.