Ping Li

The incidence of pancreatic cancer has increased slightly in recent years, coinciding with rising rates of alcohol consumption, obesity, and diabetes. According to GLOBOCAN data, approximately 496,...

Ubiquitin‑conjugating enzyme 2T (UBE2T) constitutes a critical component of the ubiquitin‑proteasome system and is involved in tumorigenesis. The UBE2T gene has been extensively characterized. In the present study, comprehensive analyses using various databases and R‑based tools revealed elevated UBE2T expression across multiple tumor types, where its upregulation was shown to be associated with poor clinical outcomes and prognosis. Gene variation analysis identified ‘amplification’ as the predominant alteration in the UBE2T gene, followed by mutations; data from the GSCALite database further demonstrated a high frequency of UBE2T copy number variations and relatively infrequent single nucleotide variants across pan‑cancer cohorts. In addition, UBE2T expression showed a positive correlation with trametinib and selumetinib sensitivity, and a negative correlation with CD‑437 and mitomycin. Moreover, UBE2T expression was shown to be significantly associated with tumor immune markers, checkpoint genes and immune cell infiltration. Functionally, elevated UBE2T expression was linked to changes in key cellular processes, including proliferation, invasion and epithelial‑mesenchymal transition. Gene Ontology, Kyoto Encyclopedia of Genes and Genomes analyses and Gene Set Enrichment Analysis implicated pathways such as ‘cell cycle’, ‘ubiquitin‑mediated proteolysis’, ‘p53 signaling’ and ‘mismatch repair’ as key mechanisms through which UBE2T may exert oncogenic effects. Overall, UBE2T has emerged as a potentially valuable prognostic biomarker and therapeutic target in oncology.

Background: Ovarian cancer (OC) is the most common malignant gynecological tumor. Cancer cells with high stemness often exhibit resistance to anti-tumor therapies, contributing to recurrence and poor prognosis. However, stemness-related subtypes in OC and their therapeutic implications remain underexplored.Methods: We identified stemness-associated genes by comparing transcriptome profiles between adherent and sphere-forming SKOV3 cells. Unsupervised clustering was applied to define stemness-related molecular subgroups in OC patients. A prognostic model was constructed using WGCNA and LASSO regression, and a nomogram was developed by integrating clinicopathological variables. Differences in the tumor microenvironment (TME), tumor mutation burden (TMB), immune checkpoint expression, and drug sensitivities were evaluated between risk groups. Single-cell RNA sequencing was used to investigate stemness-related cell types. Functional assays were conducted to validate the role of AKAP12 in OC progression.Results: Three distinct stemness-related subgroups were identified with significant differences in prognosis and immunological features. Fibroblasts were identified as major contributors to the maintenance of stemness traits in the TME. AKAP12 was found to be positively associated with stemness phenotypes. Knockdown of AKAP12 reduced tumor sphere formation, impaired cell migration, and enhanced cisplatin sensitivity. Immunohistochemistry in clinical samples and OC organoids confirmed the correlation between AKAP12 and the immune checkpoint molecule OX40L.Conclusion: This study establishes a novel stemness-related gene signature for prognosis prediction and therapeutic stratification in OC. AKAP12 was identified as a potential biomarker and therapeutic target, offering new avenues for precision treatment in stemness-driven OC.

Background: Matrix remodeling-associated 7 (MXRA7) plays a key role in physiological and pathological processes involving the extracellular matrix (ECM) and tissue remodeling. Recent studies have highlighted its functions in tissue injury, immune response, and cellular differentiation, yet no bibliometric studies have systematically mapped MXRA7 research. This study evaluates global MXRA7 research from 2015 to 2024 to identify current trends and future directions. Methods: A comprehensive bibliometric analysis was conducted using the Web of Science Core Collection. We examined publication trends, geographical contributions, influential authors, and high-impact journals, identifying research hotspots and emerging trends with advanced bibliometric tools. Results: Analysis of 553 English-language publications showed that MXRA7 research has progressed significantly after 2017, showing a general upward trend accompanied by short-term fluctuations. The United States leads, followed by China and the United Kingdom. Key studies appear in high-impact journals like PLOS ONE, and influential authors such as Wang Yiqiang have propelled the field. Keywords including “inflammation”, “extracellular matrix”, “matrix metalloproteinases” and “angiogenesis” underscore MXRA7’s roles in immune responses, tissue repair, and fibrosis. Conclusion: This analysis shows significant growth in MXRA7 research, especially in inflammation, ECM remodeling, and tissue regeneration. Future work should explore MXRA7’s molecular mechanisms in immune diseases, fibrosis, and cancer, advancing its potential as a therapeutic target.

Background: Breast cancer is the most prevalent female tumor, of which triple-negative breast cancer (TNBC) accounts for about 15%. Characterized by its aggressive nature and limited treatment options, TNBC currently stands as a significant clinical challenge. This study aimed to investigate the effects of icariin (ICA) on TNBC and explore the underlying molecular mechanism. Methods: Cell viability was assessed using CCK-8 assay, whereas the impact of ICA on cell proliferation was determined using colony formation assay and detection of proliferating cell nuclear antigen protein. Wound healing and transwell assays were used to evaluate the effects of ICA on cell migration and invasion, respectively. Flow cytometry was used to analyze cell cycle distribution and apoptosis. Transmission electron microscopy and monodansylcaverine staining were performed to detect the induction of autophagy, whereas molecular docking was conducted to predict the potential targets associated with autophagy. The in vivo anti-tumor effects of ICA were evaluated using a TNBC 4T1 xenograft mouse model. Protein expression levels were examined using immunoblotting and immunohistochemistry. Results: In vitro, ICA effectively suppressed the viability, proliferation, migration, and invasion of TNBC cells and induced G0/G1 phase cell cycle arrest, apoptosis, and autophagy in TNBC cells by regulating the adenosine monophosphate-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR)/Unc-51-like kinase 1 (ULK1) signaling pathway. The knockdown of AMPK and inhibition of autophagy with 3-methyladenine reversed the effects of ICA, highlighting the importance of AMPK and autophagy in the anti-cancer mechanism of ICA. In vivo, ICA significantly inhibited TNBC growth, promoted autophagy, and regulated AMPK/mTOR/ULK1 pathway. Conclusions: Our findings demonstrated that ICA exerts anti-cancer effects against TNBC and the associated molecular mechanisms. This study will help to facilitate further preclinical and clinical investigations for the treatment of TNBC.

Background: Stomach adenocarcinoma (STAD) is the fifth most common cancer and the third leading cause of cancer-related deaths worldwide. Cancer-testis antigens (CTAs) participate in the pathogenesis and development of multiple cancers and are aberrantly overexpressed in various types of cancer. This study aimed to develop a CTA-related gene signature (CTARSig) to predict prognosis in STAD patients and explore its underlying mechanisms.