Xiaohua Wang

Radiomics Signatures Based on Computed Tomography for Noninvasive Prediction of CXCL10 Expression and Prognosis in Ovarian Cancer

ABSTRACTBackgroundOvarian cancer (OC) is an aggressive gynecological tumor usually diagnosed with malignant ascites and even observed widespread metastasis or distant spread.AimsWe aimed to develop and identify radiomics models according to computed tomography (CT) for preoperative prediction of CXCL10 expression and prognosis in patients with OC.MethodsGenomic data with CT images and corresponding clinicopathological parameters were extracted from The Cancer Imaging Archive (TCIA) and The Cancer Genome Atlas (TCGA). To analyze the prognosis, we carried out the univariate Cox regression analysis (UCRA), multivariate Cox regression analysis (MCRA), and Kaplan–Meier (KM) analysis. For the data reduction, logistic regression, operator regression, least absolute shrinkage selection, radiomic feature construction, and feature selection were utilized. The predictive performance of the radiomic signatures was assessed using the analyses of the receiver operating characteristic (ROC) curve, decision curve (DCA), and precision‐recall (PR) curve. To evaluate the correlation between the radiomic score (Rad‐score) and CXCL10 expression, the Wilcoxon rank‐sum test was applied.ResultsThree radiomics models effectively predicted CXCL10 expression levels (AUC = 0.791, 0.748, and 0.718 for the set of training; AUC = 0.761, 0.746, and 0.701 for the set of validation). A higher Rad‐score significantly correlated with upregulated CXCL10 expression.ConclusionCXCL10 expression can be predicted noninvasively and preoperatively via radiomic signatures based on contrast‐enhanced CT images.

Artemin affects the survival and prognosis of endometrial cancer patients via regulating tumor cell proliferation

The main aim of the study is to analyze the impact of Artemin on survival and prognosis in endometrial cancer (EC) patients by bioinformatics methods. As a member of the glial-derived neurotrophic factor (GDNF) family, Artemin is not only important in the repair process of nerve damage, but also involved in tumorigenesis and metastasis. In this study, we demonstrated that Artemin mRNA was overexpressed in EC tissues. Artemin expression was closely related to the FIGO stage, pathologic differentiation, deep myometrial infiltration, lymphatic metastasis, and survival status. Univariate and multivariate Cox regression analysis showed that ectopic overexpression of Artemin predicted poor survival prognosis. Artemin expression could be used as an independent risk factor for the prognosis of EC patients. The proliferation of EC cells was significantly downregulated by silencing of Artemin. Artemin promotes tumor progression by regulating the proliferation of EC cells, thereby affecting the prognosis of EC patients.

CST2 promotes cell proliferation and regulates cell cycle by activating Wnt-β-catenin signalling pathway in serous ovarian cancer

Cystatin SA (CST2) plays multiple roles in different types of malignant tumours; however, its role in serous ovarian cancer (SOC) remains unclear. Therefore, we aimed to investigate the expression levels, survival outcomes, immune cell infiltration, proliferation, cell cycle, and underlying molecular mechanisms associated with the CST2 signature in SOC. The Cancer Genome Atlas database was used to acquire clinical information and CST2 expression profiles from patients with SOC. Wilcoxon rank-sum tests were used to compare CST2 expression levels between SOC and normal ovarian tissues. A prognostic assessment of CST2 was conducted using Cox regression analysis and the Kaplan-Meier method. Differentially expressed genes were identified using functional enrichment analysis. Immune cell infiltration was examined using a single-sample gene set enrichment analysis. Cell cycle characteristics and proliferation were assessed using a colony formation assay, flow cytometry, and a cell counting kit-8 assay. Western blots and quantitative reverse transcription PCR analyses were employed to examine CST2 expressions and related genes involved in the cell cycle and the Wnt-β-catenin signalling pathway. Our findings revealed significant upregulation of CST2 in SOC, and elevated CST2 expression was correlated with advanced clinicopathological characteristics and unfavourable prognoses. Pathway enrichment analysis highlighted the association between the cell cycle and the Wnt signalling pathway. Moreover, increased CST2 levels were positively correlated with immune cell infiltration. Functionally, CST2 played vital roles in promoting cell proliferation, orchestrating the G1-to-S phase transition, and driving malignant SOC progression through activating the Wnt-β-catenin signalling pathway. The elevated expression of CST2 may be related to the occurrence and progression of SOC by activating the Wnt-β-catenin pathway. Additionally, our findings suggest that CST2 is a promising novel biomarker with potential applications in therapeutic, prognostic, and diagnostic strategies for SOC.