RÉSUMÉ
Bladder cancer is one of the most prevalent cancers worldwide, and its morbidity and mortality rates have been increasing over the years. However, how RAC family small GTPase 3 (RAC3) affects the proliferation, migration and invasion of cisplatin-resistant bladder cancer cells remains unclear. Bioinformatics techniques were used to investigate the expression of RAC3 in bladder cancer tissues. Influences of RAC3 in the grade, stage, distant metastasis, and survival rate of bladder cancer were also examined. Analysis of the relationship between RAC3 expression and the immune microenvironment (TIME), genomic mutations, and stemness index. In normal bladder cancer cells (T24, 5637, and BIU-87) and cisplatin-resistant bladder cancer cells (BIU-87-DDP), the expression of RAC3 was detected separately with Western blotting. Plasmid transfection was used to overexpress or silence the expression of RAC3 in bladder cancer cells resistant to cisplatin (BIU-87-DDP). By adding activators and inhibitors, the activities of the JNK/MAPK signalling pathway were altered. Cell viability, invasion, and its level of apoptosis were measured in vitro using CCK-8, transwell, and flow cytometry. The bioinformatics analyses found RAC3 levels were elevated in bladder cancer tissues and were associated with a poor prognosis in bladder cancer. RAC3 in BIU-87-DDP cells expressed a higher level than normal bladder cancer cells. RAC3 overexpression promoted BIU-87-DDP proliferation. The growth of BIU-87-DDP cells slowed after the knockdown of RAC3, and RAC3 may have had an impact on the activation of the JNK/MAPK pathway.
Sujet(s)
Apoptose , Mouvement cellulaire , Prolifération cellulaire , Cisplatine , Résistance aux médicaments antinéoplasiques , Régulation de l'expression des gènes tumoraux , Invasion tumorale , Tumeurs de la vessie urinaire , Protéines G rac , Humains , Tumeurs de la vessie urinaire/anatomopathologie , Tumeurs de la vessie urinaire/génétique , Tumeurs de la vessie urinaire/métabolisme , Tumeurs de la vessie urinaire/traitement médicamenteux , Cisplatine/pharmacologie , Résistance aux médicaments antinéoplasiques/génétique , Lignée cellulaire tumorale , Protéines G rac/métabolisme , Protéines G rac/génétique , Apoptose/effets des médicaments et des substances chimiques , Régulation de l'expression des gènes tumoraux/effets des médicaments et des substances chimiques , Femelle , Mâle , Adulte d'âge moyen , Microenvironnement tumoral , Système de signalisation des MAP kinases/effets des médicaments et des substances chimiquesRÉSUMÉ
OBJECTIVE: We aimed to investigate the diagnostic value of different laboratory indicators in combination with total prostate-specific antigen (TPSA) for prostate cancer (PCa). METHODS: In this retrospective study, we selected 291 patients who underwent prostate biopsy. Patients were divided into the benign prostatic hyperplasia group and the PCa group. In both groups, patients were again divided into a group with TPSA 4.0-10.0 ng/mL and a group with TPSA >10.0 ng/mL. Clinical data including age, pre-puncture TPSA, free prostate-specific antigen (FPSA), and prostate volume (PV) were collected from all patients. We calculated the metrics PSA/PV (prostate-specific antigen density, PSAD), age/PV (AVR), age × PV/TPSA (PSA-AV), and (FPSA/TPSA)/PSAD [(F/T)/PSAD]). We plotted receiver operating characteristic (ROC) curves and calculated the area under the ROC curve (AUC). RESULTS: We found statistically significant differences in PV, PSAD, AVR, PSA-AV, and (F/T) PSAD for patients with TPSA 4.0-10.0 ng/mL and TPSA >10 ng/mL. We further plotted the ROC of individual or combined indices in different subgroups and calculated the AUC. We found that the diagnostic efficacy of the combined indices was higher with TPSA >10 ng/mL. CONCLUSION: The combination of TPSA with multiple indicators may improve diagnostic accuracy for PCa.
Sujet(s)
Hyperplasie de la prostate , Tumeurs de la prostate , Mâle , Humains , Antigène spécifique de la prostate , Études rétrospectives , Tumeurs de la prostate/diagnostic , Tumeurs de la prostate/anatomopathologie , Prostate/anatomopathologie , Hyperplasie de la prostate/diagnostic , Hyperplasie de la prostate/anatomopathologie , Courbe ROCRÉSUMÉ
The moving averaging-moving differential (MA-MD) algorithm is widely adopted for event recognition and positioning in phase-sensitive optical time-domain reflectometry (Φ-OTDR) vibration sensing. In this paper, two theorems about the two critical parameters of this algorithm, the MA window width and the MD interval, are found, proved, and verified. According to them we can not only obtain an optimal signal-to-noise ratio and avoid missing the vibration signal but also greatly improve the signal-searching efficiency. Work in this paper is of essential importance for understanding the characteristics of the MA-MD algorithm and will remarkably benefit its practical applications.