Correlation analysis of disulfidptosis-related gene signatures with clinical prognosis and immunotherapy response in sarcoma.

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.

Tobacco nicotine promotes TRAIL resistance in lung cancer through SNHG5.

Tobacco nicotine use is carcinogenic and a well-known risk factor for lung cancer. However, whether tobacco nicotine can induce drug resistance in lung cancer is not clear. The objective of the present study was to identify the TNF-related apoptosis-inducing ligand (TRAIL) resistance of long noncoding RNAs (lncRNAs) that are differentially expressed in smokers and nonsmokers with lung cancer. The results suggested that the nicotine upregulated small nucleolar RNA host gene 5 (SNHG5) and markedly decreased the levels of cleaved caspase-3. The present study found that cytoplasm lncRNA SNHG5 overexpression was associated with TRAIL resistance in lung cancer and that SNHG5 can interact with X-linked inhibitor of apoptosis protein to promote TRAIL resistance. Therefore, nicotine promoted TRAIL resistance in lung cancer through SNHG5/X-linked inhibitor of apoptosis protein.

Expression and clinical significance of Vimentin and E-cadherin in breast cancer tissues / 中国肿瘤生物治疗杂志

@#Objective: To study the expression and clinical significance of Vimentin and E-cadherin in human breast cancer tissues. Methods: : The clinical data of 56 cases of breast cancer patients, who underwent radical mastectomy in Chaohu Hospital Affiliated to Anhui Medical University from January 2014 to January 2016, were retrospectively analyzed. The protein and mRNAexpressions of Vimentin and E-cadherin in breast cancer tissues were detected by immunohistochemistry and qPCR, respectively; and the relationship between the expression of Vimentin and E-cadherin in breast cancer tissues and the clinicopathological characteristics was analyzed. Logistic multivariate regression was used to analyze the independent factors affecting the protein expressions of Vimentin and E-cadherin. Spearman was used to analyze the correlation between Vimentin and E-cadherin. Kaplan-Meier was used to analyze the relationship between protein expressions of Vimentin, E-cadherin and prognosis. ROC curve was used to analyze the diagnostic value of Vimentin and E-cadherin on prognosis. Results: The rates of breast cancer tissues with high positive expression of Vimentin and E-cadherin were 76.79% and 19.64%, respectively.Among them, 47 cases (47/56, 83.93%) of breast cancer tissues showed significantly higher Vimentin mRNA expression than adjacent tissues (P<0.05), and 46 cases (46/56, 82.14%) of breast cancer tissues showed significantly lower Ecadherin mRNA expression than adjacent tissues (P<0.05). Vimentin protein expression was associated with tumor size, lymph node metastasis, vascular invasion, histological grade, clinical stage, molecular typing, Ki67+, ER-, PR- and HER2- expression (P<0.05). And E-cadherin protein expression was associated with lymph node metastasis, vascular invasion, histological grade, clinical stage, molecular typing, Ki67+, ER-, PR- and HER2- expression (P<0.05). Tumor size, lymph node metastasis, vascular invasion, histological grading, clinical staging, molecular typing, Ki67+, ER-, PR- and HER2- expression were all independent factors affecting the expression of Vimentin and E-cadherin (P<0.05). There was a negative correlation between Vimentin and E-cadherin expression (P<0.05). The 3-year survival rate of patients with high expression of Vimentin protein was 67.44%, while that of patients with low expression of E-cadherin protein was 68.89%. Conclusion: The high expression of Vimentin and low expression of E-cadherin in breast cancer tissues may be related to the occurrence, development, invasion and metastasis of breast cancer. It can be used as a reliable indicator of clinical diagnosis and prognosis.