Background: Osteosarcoma (OS) is a common severe illness globally. Lupeol has been reported to participate in the pathophysiologic properties of various cancers, including OS. This study aimed to explore the effects of lupeol on proliferation, invasion, and apoptosis on OS cells and the underlying mechanism. Methods: The cell viability of OS cells was determined by 3-(4, 5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay. The expression levels of miR-212-3p and high-mobility group AT-hook 2 (HMGA2) were detected by quantitative real-time polymerase chain reaction (qRT-PCR) in OS cells. The cell apoptosis and invasion were detected by flow cytometry and transwell invasion assays, respectively. The functional target of miR-212-3p was predicted by online software and confirmed by luciferase reporter assay. The protein level of HMGA2 was measured by western blot analysis. Results: Lupeol suppressed cell viability and invasion, and promoted apoptosis by upregulating the expression of miR-212-3p in OS cells. Knockdown of miR-212-3p restored the anti-tumor effect of lupeol. Interestingly, miR-212-3p directly targeted HMGA2 and suppressed its expression. Moreover, HMGA2 reversed the inhibited impact on viability and invasion, and the promoted effect on apoptosis induced by upregulation of miR-212-3p. Also, lupeol administration exerts its anti-tumor effect by overexpression of miR-212-3p to suppress the expression of HMGA2 in OS cells. Conclusion: Lupeol inhibited OS progression by modulating the miR-212-3p/HMGA2 axis in vitro.

Tongue squamous cell carcinoma (TSCC) is one of the deadliest cancers of the head and neck, but the role of the ferroptosis pathway in its development is still unknown. In this study we explored the pathogenetic mechanisms associated with ferroptosis in TSCC. We identified differentially expressed genes (DEGs) of TSCC patients and used gene ontology (GO), the Kyoto Encyclopedia of Genes and Genomes (KEGG), and gene set enrichment analysis (GSEA) to annotate, visualize, and integrate these DEGs. Receiver operating characteristic curve (ROC) analysis was performed, and the STRING database was used to construct a protein–protein interaction network to evaluate the predictive value of ferroptosis‐related DEGs. A total of 219 DEGs were identified and GO, KEGG, and GSEA showed that extracellular matrix (ECM)‐receptor interaction and interleukin (IL)‐17 signaling pathways were substantially upregulated in TSCC. Univariate Cox analysis revealed that high expression of CA9, TNFAIP3, and NRAS were predictive of a worse outcome. We then constructed a prognostic model that predicted survival in the validation cohort at 1 year and 32 months. Finally, 60 cases of tongue carcinoma and normal tissues were collected, and immunohistochemistry was used to detect the expression of CA9. We found that CA9 was strongly expressed in tongue carcinoma tissues and absent in adjacent tissues. Overall, we found that ferroptosis‐related genes may affect TSCC prognosis through the ECM‐receptor interaction and IL‐17 signaling pathways. Additionally, immunohistochemistry confirmed that CA9 was highly expressed in tongue carcinoma tissues, and a model based on ferroptosis‐related genes showed a good ability to predict overall survival in TSCC.

Gastric cancer, a prevalent malignancy, often presents challenges due to its low early diagnosis rate and poor prognosis. This study aims to establish a prognostic model composed of genes from the CLEC family, aiming to predict the prognosis of gastric cancer patients effectively. Data Collection: mRNA expression matrices and clinical data were downloaded from the TCGA, GEO, and GTEx databases. Differential analysis, univariate Cox analysis, lasso regression analysis, and multivariate Cox analysis were conducted to identify three genes associated with the prognosis of the CLEC family for building a prognostic model. Prognostic Model Construction: A prognostic model comprising these three genes was constructed. The prognostic value was evaluated using Kaplan–Meier plots, time-dependent receiver operating characteristic curves, multivariable Cox regression analysis incorporating clinical information, and a nomogram. The predictive value of the three-gene signature was further validated using the GSE84437 dataset. Immune and Functional Analyses: Differences in immune status and signaling pathways between different risk groups were assessed through analyses of the tumor microenvironment, immune cell infiltration, immune function, and gene set enrichment. Through tumor mutation analysis, the molecular mechanisms of tumors were revealed. Finally, chemotherapy-sensitivity drugs were identified through drug analysis. Results revealed CD93, CLEC3A, and VCAN as three CLEC family genes associated with prognosis. Multivariable Cox regression analysis demonstrated that these three CLEC family genes were independent prognostic factors for overall survival in gastric cancer patients. Additionally, we constructed a prognostic nomogram that incorporated risk score, age, grade, and stage. Based on TCGA/GSE84437 data, calibration plots demonstrated its predictive solid performance. Furthermore, immune-related analyses and drug sensitivity assessments suggested a close association between the three-gene model and immune cell infiltration, indicating their potential as predictive indicators for chemotherapy sensitivity. We have identified a CLEC family gene model consisting of three genes associated with the prognosis of gastric cancer. This provides a basis for personalized prevention and treatment strategies.

To analyze the effect of jaw width in jaw tracking mode on the dose of radiotherapy partial arc VMAT (P-VMAT) for patients undergoing left breast-conserving surgery and to explore the best jaw width as the initial inverse optimization parameter. Twenty patients who underwent left breast-conserving surgery were randomly selected. Six groups of P-VMAT plans were designed (named Plan0, Plan0.3, Plan0.6, Plan0.9, Plan-0.3, and Plan-0.6). The width of the jaw of each plan was changed in 0.3 cm steps along the X direction (from − 0.6 to 0.9 cm) according to the beginning of the half beam (Plan0). The PTV coverage, conformity index (CI), homogeneity index (HI), monitor units (MU) and organs at risk (OARs) dose were evaluated by repeated measurement data analysis of variance between plan0 and the other plans. Additionally, the correlations between CI, HI, MU and OARs to change in jaw width were analyzed using Spearman’s bivariate correlation analysis. The PTV dose distributions of Plan-0.3 and Plan-0.6, which have smaller jaw widths than those of Plan0, did not meet the clinical requirements. CI, HI and MU were correlated with jaw width (r = 0.554, -0.501, -0.641, p < 0.05, respectively). The V5, V10, V20, V40, Dmean and Dmax of the heart were correlated with jaw width (r = 0.288, 0.284, 0.191, -0.27, 0.186, -0.245, p < 0.05, respectively). The V2.5, V5, V10, V20, V40 and Dmean of the left lung (Lung-L) were correlated with jaw width (0.298, 0.421, 0.516, 0.391, -0.241, 0.356, p < 0.05, respectively). Among all the plans to ensure PTV target coverage, Plan0 had the lowest clinical indicators for the heart and Lung-L (p < 0.05, respectively). The internal boundary of the jaw set as 0 cm (Plan0) represents the optimal jaw width for the initial optimization of the plan design. This method is the simplest and most effective for radiotherapy treatment planning for breast-conserving surgery for breast cancer as well as allows ideal dose distribution.

To evaluate the efficacy of surface-guided radiation therapy (SGRT) combined with real-time position management (RPM)-guided deep inspiratory breath-hold (

Objective To investigate the expression and correlation of COX-2 and NUCB1 in colorectal adenocarcinoma and adjacent tissues. Methods The expression of COX-2 and NUCB1 and their effects on prognosis were predicted using bioinformatics. Immunohistochemistry was used to identify the expression of two molecules in 56 cases of colorectal adenocarcinoma and the surrounding tissues. The expression of two molecules and their association with clinicopathological variables were examined using the chi-square test. The association between COX-2 and NUCB1 was investigated using the Spearman correlation test. Results The STRING database revealed that COX-2 and NUCB1 were strongly linked. According to the UALCAN and HPA database, COX-2 was upregulated while NUCB1 was downregulated in colorectal adenocarcinoma, both at the protein and gene levels. The OS times for COX-2 and NUCB1 high expression, however, exhibited the same patterns. The rate of positive COX-2 immunohistochemical staining in cancer tissues was 69.64% (39/56), which was significantly higher than the rate in healthy tissues 28.57% (16/56). NUCB1 was expressed positively in cancer tissues at a rate of 64.29% (36/56) compared to just 19.64% (11/56) in neighboring tissues. The positive expression levels of COX-2 and NUCB1 were both closely related to clinical stage, differentiation degree, and lymphatic metastases (P < 0.05). In colorectal cancer, COX-2 and NUCB1 expression were significantly correlated (r_s = 0.6312, P < 0.001). Conclusion Both COX-2 and NUCB1 are overexpressed and significantly associated in colorectal adenocarcinoma.