Background. Breast cancer is the frequent cause of disease burden related to cancer among women. It affects one in 20 women globally and up to one in eight women in high-income countries. Cuproptosis is a copper-induced modality of mitochondrial cell death that is involved in tumor proliferation and metastasis. Methods. To construct a prognostic cuproptosis-related signature, LASSO Cox regression analysis was employed. Additionally, ceRNA was developed with an aim of exploring the possible lncRNA-miRNA-mRNA regulatory axis in breast cancer. Results. The expression of FDX1, DLD, DLAT, LIAS, LIPT1, GLS MTF1, and PDHA1 was downregulated, while CDKN2A expression level was elevated in breast cancer in contrast with normal tissue. We furthermore reviewed the genetic mutation landscape of genes linked to cuproptosis in breast cancer. Prognosis analysis revealed poor OS and RFS rates in breast cancer patients with elevated levels of CDKN2A and PDHA1 and low levels of MTF1, DLD, LIPT1, and FDX1. We then constructed a cuproptosis-related signature with six genes (DKN2A, MTF1, PDHA1, DLD, LIPT1, and FDX1) for breast cancer, which predicted the OS rate with an accuracy that ranged from medium to high. Further analysis demonstrated a significant correlation between the cuproptosis-related prognostic signature and pTNM stage, MSI score, drug sensitivity, TMB score, and immune cell infiltration. Moreover, we identified the lncRNA XIST/miR-92b-3p/MTF1 regulatory axis for breast cancer. Conclusion. Multiomics approaches were used to create a cuproptosis-related signature with six genes (DKN2A, MTF1, PDHA1, DLD, LIPT1, and FDX1) for breast cancer. We discovered the lncRNA XIST/miR-92b-3p/MTF1 regulatory axis for breast cancer, which has not yet been investigated previously.

The aim of this study was to develop and validate a radiomics nomogram based on radiomics features and clinical data for the non-invasive preoperative prediction of early recurrence (≤2 years) in patients with hepatocellular carcinoma (HCC). We enrolled 262 HCC patients who underwent preoperative contrast-enhanced computed tomography and curative resection (training cohort, n=214; validation cohort, n=48). We applied propensity score matching (PSM) to eliminate redundancy between clinical characteristics and image features, and the least absolute shrinkage and selection operator (LASSO) was used to prevent overfitting. Next, a radiomics signature, clinical nomogram, and combined clinical-radiomics nomogram were built to predict early recurrence, and we compared the performance and generalization of these models. The radiomics signature stratified patients into low-risk and high-risk, which show significantly difference in recurrence free survival and overall survival (P ≤ 0.01). Multivariable analysis identified dichotomised radiomics signature, alpha fetoprotein, and tumour number and size as key early recurrence indicators, which were incorporated into clinical and radiomics nomograms. The radiomics nomogram showed the highest area under the receiver operating characteristic curve (AUC), with significantly superior predictive performance over the clinical nomogram in the training cohort (0.800 vs 0.716, respectively; P = 0.001) and the validation cohort (0.785 vs 0.654, respectively; P = 0.039). The radiomics nomogram is a non-invasive preoperative biomarker for predicting early recurrence in patients with HCC. This model may be of clinical utility for guiding surveillance follow-ups and identifying optimal interventional strategies.

Thyroid cancer is the most common form of endocrine cancer around the world, and among which papillary thyroid carcinoma (PTC) is the most ubiquitous pathological sub-kind. Sushi repeat-containing protein X-linked 2 (SRPX2) was reported to be an independent prognostic factor and significantly overexpressed in advanced PTC patients. However, the biological functions of SRPX2 remain ambiguous in PTC. Here, we explored SRPX2 expression profiles and functions in PTC, finding that SRPX2 expression was remarkably upregulated in PTC tissues and cell lines. Further colony formation, CCK-8, as well as transwell assay, suggested that SRPX2 silencing remarkably dampened PTC growth and migration. Mouse xenograft models were established to find that SRPX2 silence remarkably suppressed PTC proliferation and migration in vivo. Following mechanism studies revealed that SRPX2 realized its functions in the PTC process partially through activating the Focal adhesion kinase (FAK) phosphorylation. In conclusion, this study investigated the functions and mechanisms of the SRPX2/FAK pathway in PTC progression. SRPX2 could act as a prospective biologic signature and therapeutic target molecule for PTC.