Cystadenomas of the seminal vesicles are extremely rare. Here, we report a large seminal vesicle cystadenoma. A 37‐year‐old man presented a 6‐month history of haemospermia, 10 days of Lower Urinary Tract symptoms (LUTSs) and gross haematuria. Transabdominal ultrasonography, computed tomography and magnetic resonance imaging were performed and revealed a large solid‐cystic pelvic mass morphometrically measured 7.0 cm × 11.9 cm × 8.6 cm on the right seminal vesicle, which caused hydronephrosis of the right kidney. The prostate‐specific antigen of the patient was 27.860 ng/dl. Laparoscopic exploration found the capsule of tumour was complete and the tumour came from the right seminal vesicle, in addition, the mass had a certain space with the bladder and prostate, which could be separated. So a nerve‐sparing Laparoscopic Vesiculectomy was performed at last, even though the intraoperative frozen section analysis could not make sure the nature of the tumour either. The postoperative pathology revealed cystadenoma of the seminal vesicle.
Background: Aberrantly autophagy and preternatural elevated glycolysis are prevalent in bladder cancer (BLCA), which are both related to malignant progression. But the regulatory relationship between autophagy and glycolytic metabolism remains unveiled. We imitated a starvation condition of tumor microenvironment and found significantly increased level of autophagy and aerobic glycolysis, which both regulated progression of BLCA cells. We further explored regulatory relationships and mechanisms between them.Methods: We used immunoblotting, immunofluorescence and transmission electron microscopy to detect autophagy levels of BLCA cells under different treatment. Lactate and glucose concentration detection demonstrated changes on glycolysis. Expression of lactate dehydrogenase A (LDHA) were detected at transcriptional and translational levels, which were also silenced by small interfering RNA and effects on malignant progression further tested. Underlying mechanisms on signaling pathways were performed by western blot, immunofluorescence and immunoprecipitation assays.Results: Starvation induced autophagy, regulated glycolysis by up-regulating expression of LDHA and caused progressive changes in BLCA cells. Mechanically, after starved ubiquitination modification of Axin1 increased and combined with P62, further degraded by autophagy-lysosome pathway. Liberated β-catenin nuclear translocation increased, binding with LEF1/TCF4 and promotes LDHA transcriptional expression. Also, high expression of LDHA was observed in cancer tissues and positively related to progression.Conclusion: Our study demonstrated that starvation-induced autophagy modulates glucose metabolic reprogramming by enhances Axin1 degradation and β-catenin nuclear translocation in BLCA, which promotes transcriptional expression of LDHA and further malignant progression.
Clear cell renal cell carcinoma (ccRCC) is one of the most common cancer types worldwide, and its incidence is increasing year by year. Endoplasmic reticulum stress (ERS) caused by protein misfolding has broad and profound effects on the progression and metastasis of various cancers. Accumulating evidence suggests that ERS-related genes are closely related to the occurrence and progression of ccRCC. This study aimed to identify ERS-related signature genes for evaluating the prognosis of ccRCC patients. Transcriptomic expression profiles of patients with ccRCC from public databases Gene Expression Omnibus (GEO) and the Cancer Genome Atlas (TCGA) and survival data and clinical phenotype data of patients in the TCGA database were used. Then the GeneCards database was used to identify the differentially expressed genes related to ERS. We obtained 11 signature genes, and then used the Lasso regression method to establish a diagnostic model, univariate and multivariate Cox analysis was used to analyze the correlation between the expression levels of the signature genes and the clinical characteristics, and finally 5 signature genes were associated with poor prognosis (TNFSF13B, APOL1, COL5A3, CDH5). In summary, this study suggests that these genes may have potential as prognostic biomarkers in ccRCC and may provide new evidence to support targeted therapy in ccRCC.
Background: Bladder cancer is one of the most prevalent malignancies worldwide. However, traditional indicators have limited predictive effects on the clinical outcomes of bladder cancer. The aim of this study was to develop and validate a glycolysis-related gene signature for predicting the prognosis of patients with bladder cancer that have limited therapeutic options. Methods: mRNA expression profiling was obtained from patients with bladder cancer from The Cancer Genome Atlas (TCGA) database. Gene set enrichment analysis (GSEA) was conducted to identify glycolytic gene sets that were significantly different between bladder cancer tissues and paired normal tissues . A prognosis-related gene signature was constructed by univariate and multivariate Cox analysis. Kaplan-Meier curves and time-dependent receiver operating characteristic (ROC) curves were utilized to evaluate the signature. A nomogram combined with the gene signature and clinical parameters was constructed. Correlations between glycolysis-related gene signature and molecular characterization as well as cancer subtypes were analyzed. RT-qPCR was applied to analyze gene expression. Functional experiments were performed to determine the role of PKM2 in the proliferation of bladder cancer cells. Results: Using a Cox proportional regression model, we established that a 4-mRNA signature (NUP205, NUPL2, PFKFB1 and PKM) was significantly associated with prognosis in bladder cancer patients. Based on the signature, patients were split into high and low risk groups, with different prognostic outcomes. The gene signature was an independent prognostic indicator for overall survival. The ability of the 4-mRNA signature to make an accurate prognosis was tested in two other validation datasets. GSEA was performed to explore the 4-mRNA related canonical pathways and biological processes, such as the cell cycle, hypoxia, p53 pathway, and PI3K/AKT/mTOR pathway. A heatmap showing the correlation between risk score and cell cycle signature was generated. RT-qPCR revealed the genes that were differentially expressed between normal and cancer tissues. Experiments showed that PKM2 plays essential roles in cell proliferation and the cell cycle. Conclusion: The established 4‑mRNA signature may act as a promising model for generating accurate prognoses for patients with bladder cancer, but the specific biological mechanism needs further verification.
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