RNA modifications are reversible, dynamically regulated, and involved in a variety of diseases such as cancers. Given the lack of efficient and reliable biomarkers for early diagnosis of ovarian cancer (OV), this study was designed to explore the role of RNA modification genes (RMGs) in the diagnosis of OV. Herein, 132 RMGs were retrieved in PubMed, 638 OV and 18 normal ovary samples were retrieved in The Cancer Genome Atlas (TCGA), and GSE18520 cohorts were collected for differential analysis. Finally, PUS7 (Pseudouridine Synthase 7) as differentially expressed RMGs (DEGs-RMGs) was identified as a diagnostic biomarker candidate and evaluated for its specificity and sensitivity using Receiver Operating Characteristic (ROC) analysis in TCGA and GEO data. The protein expression, mutation, protein interaction networks, correlated genes, related pathways, biological processes, cell components, and molecular functions of PUS7 were analyzed as well. The upregulation of PUS7 protein in OV was confirmed by the staining images in HPA and tissue arrays. Collectively, the findings of the present study point towards the potential of PUS7 as a diagnostic marker and therapeutic target for ovarian cancer.

Abnormal expression and dysfunction of Annexins (ANXA1-11, 13) have been widely found in several types of cancer. However, the expression pattern and prognostic value of Annexins in bladder cancer (BC) are currently still unknown. In this study, survival analysis by our in-house OSblca web server revealed that high ANXA1/2/3/5/6 expression was significantly associated with poor overall survival (OS) in BC patients, while higher ANXA11 was associated with increased OS. Through Oncomine and GEPIA2 database analysis, we found that ANXA2/3/4/13 were up-regulated, whereas ANXA1/5/6 were down-regulated in BC compared with normal bladder tissues. Further LASSO analysis built an Annexin-Related Prognostic Signature (ARPS, including four members ANXA1/5/6/10) in the TCGA BC cohort and validated it in three independent GEO BC cohorts (GSE31684, GSE32548, GSE48075). Multivariate COX analysis demonstrated that ARPS is an independent prognostic signature for BC. Moreover, GSEA results showed that immune-related pathways, such as epithelial–mesenchymal transition and IL6/JAK/STAT3 signaling were enriched in the high ARPS risk groups, while the low ARPS risk group mainly regulated metabolism-related processes, such as adipogenesis and bile acid metabolism. In conclusion, our study comprehensively analyzed the mRNA expression and prognosis of Annexin family members in BC, constructed an Annexin-related prognostic signature using LASSO and COX regression, and validated it in four independent BC cohorts, which might help to improve clinical outcomes of BC patients, offer insights into the underlying molecular mechanisms of BC development and suggest potential therapeutic targets for BC.

Blood group antigen is a class of heritable antigenic substances present on the erythrocyte membrane. However, the role of blood group antigens in cancer prognosis is still largely unclear. In this study, we investigated the expression of 33 blood group antigen genes and their association with the prognosis of 30 types of cancers in 31,870 tumor tissue samples. Our results revealed that blood group antigens are abnormally expressed in a variety of cancers. The high expression of these antigen genes was mainly related to the activation of the epithelial-mesenchymal transition (EMT) pathway. High expression of seven antigen genes, i.e., FUT7, AQP1, P1, C4A, AQP3, KEL and DARC, were significantly associated with good OS (Overall Survival) in six types of cancers, while ten genes, i.e., AQP1, P1, C4A, AQP3, BSG, CD44, CD151, LU, FUT2, and SEMA7A, were associated with poor OS in three types of cancers. Kidney renal clear cell carcinoma (KIRC) is associated with the largest number (14 genes) of prognostic antigen genes, i.e., CD44, CD151, SEMA7A, FUT7, CR1, AQP1, GYPA, FUT3, FUT6, FUT1, SLC14A1, ERMAP, C4A, and B3GALT3. High expression of SEMA7A gene was significantly correlated with a poor prognosis of KIRC in this analysis but has not been reported previously. SEMA7A might be a putative biomarker for poor prognosis in KIRC. In conclusion, our analysis indicates that blood group antigens may play functional important roles in tumorigenesis, progression, and especially prognosis. These results provide data to support prognostic marker development and future clinical management.

Cholangiocarcinoma (CCA) is a malignant tumor arising from the epithelial cells of the biliary tract. It is characterized by high heterogeneity, frequent late diagnosis, high rates of metastasis, and overall poor prognosis. Unfortunately, the development of sensitive biomarkers and effective therapeutic approaches remains challenging and an unmet need. In recent years, advances in molecular biological techniques have significantly enhanced our understanding of the molecular mechanisms underlying CCA pathogenesis. This review summarized the biomarkers identified in CCA, highlighted the critical genes and signal transduction pathways closely associated with tumor cell proliferation and migration, inflammation regulation, angiogenesis, and tumor microenvironment, and discussed the complex regulatory roles of epigenetic alterations in CCA initiation and progression. These recent insights not only deepen our understanding of the molecular complexity of CCA but also lay a solid foundation for the development of precision medicine and individualized therapeutic strategies for patients with this aggressive malignancy.

Kidney renal clear cell carcinoma (KIRC) is a prevalent histological subtype of kidney cancer and one of the most invasive urinary tumors. Members of the cullin family play a pivotal role in driving the development and progression of neoplasms. Accumulating evidence suggests that cullins might play a significant part in the initiation and advancement of KIRC. In this study, the messenger ribonucleic acid expression profiles for eight members of the cullin family (CUL1 – 9) were noticeably upregulated in KIRC compared to normal tissue, whereas CUL3, CUL5, and CUL7 were downregulated. Moreover, our analysis demonstrated that higher expression levels of CUL1 – 3, CUL4A, CUL4B, CUL5, and CUL7 were significantly correlated with enhanced overall survival (OS) in KIRC patients. Co-expression gene analysis showed that the differential expression of cullins in KIRC was predominantly associated with 20 genes. Functional enrichment analysis indicated that cullins in KIRC primarily participated in ubiquitin-mediated protein degradation, facilitated protein polyubiquitylation, and regulated APC/C activators during the G1/S phase transition and early anaphase. Furthermore, cullin gene expression exhibited a positive correlation with the activity of tumor-infiltrating immune cells. These findings suggest that cullins may serve as diagnostic and prognostic biomarkers in KIRC patients.