Renal cell carcinoma (RCC) is a common urological malignancy. Circular RNAs (circRNAs) have been confirmed to play an important regulatory role in various cancers. This study aimed to investigate the role and potential mechanism of circTLK1 (hsa_circ_0004442) in RCC. The levels of circTLK1, Cbl proto-oncogene (CBL), and microRNA-495-3p (miR-495-3p) were detected by quantitative reverse transcription polymerase chain reaction or western blot. Cell proliferation, cycle arrest and apoptosis, migration, and invasion were assessed by colony formation, flow cytometry, scratch, and transwell assays. The levels of E-cadherin and Vimentin were measured by western blot. The targeting relationship between miR-495-3p and miR-495-3p or CBL was verified by dual-luciferase reporter assay. Tumor growth in vivo was evaluated by xenograft assay. The results found that circTLK1 and CBL were up-regulated in RCC tissues and cells. Silencing of circTLK1 or CBL inhibited proliferation and metastasis and accelerated apoptosis in RCC cells. In addition, circTLK1 directly bound to miR-495-3p, and CBL was the target of miR-495-3p. circTLK1 sponged miR-495-3p to increase CBL expression. Moreover, knockdown of circTLK1 suppressed tumor growth in vivo. In conclusion, down-regulation of circTLK1 restrained proliferation and metastasis and promoted apoptosis in RCC cells by modulating miR-495-3p/CBL axis.

Objective. The objective of the study was to determine if acute kidney injury (AKI) in patients with acute ischemic stroke was associated with the monocyte-to-lymphocyte ratio (MLR) assessed upon admission to the neurology intensive care unit (NICU) (AIS). We also looked into the MLR’s function in predicting hospital mortality in AIS patients. Methods. This retrospective analysis included 595 adult patients with AIS who were hospitalized to the NICU of the First Affiliated Hospital of South China between January 2017 and December 2019. Clinical signs and imaging studies were used to diagnose AIS. KDIGO criteria were used to define AKI. The ratio of monocytes to lymphocytes was used to compute MLR, the ratio of neutrophils to lymphocytes was used to calculate NLR, and the ratio of platelets to lymphocytes was used to calculate PLR. Result. 361 males and 234 women between the ages of 66.27 ± 12.05 years took part in the study. The individuals’ MLR was 0.4729 ± 0.3461 and their neutrophil-to-lymphocyte ratio (NLR) was 8.18 ± 5.45 . There were notable disparities in MLR and NLR between the AKI and non-AKI groups ( p < 0.001 ). The link between MLR and AKI development risk was enhanced after adjustment, with respective cutoff values of 0.4581 and 9.26. For the MLR-based prediction of AKI incidence, the areas under the receiver-operating characteristic curves (AUCs) were 0.711 (95% CI: 0.663-0.758). And NLR-based prediction of AKI incidence the AUCs was (95% CI: 0.742-0826). Additionally, MLR was associated with a higher rate of in-hospital mortality (2.825, 95% confidence interval: 1.058, 7.545), whereas NLR was associated with a risk of in-hospital mortality of 1.085. (95 percent CI: 1.022, 1.151). An AUC of 0.745 (95% CI: 0.601-0.889, p = 0.026 ) was obtained for in-hospital mortality based on the MLR, whereas an AUC of 0.724 (95% CI: 0.531-0.916, p = 0.042 ) was obtained for in-hospital mortality based on the NLR. Conclusion. MLR and neutrophil-to-lymphocyte ratio (NLR) were associated with a higher risk of AKI and in-hospital death in AIS patients.

Small nucleolar RNA host gene 16 (SNHG16) participates in some cancers as microRNA (miR)-1303 is also reported to function on proliferation of various cancer cells. This study aimed to assess SNHG16 and miR-1303′s role in renal cell carcinoma (RCC) and its underlying mechanism. RT-qPCR was used to determine SNHG16 and miR-1303 expression in RCC cells (A498, 786-O, ACHN and OS-RC-2) and normal kidney epithelial cells (HK-2). Functional experiment was established to detect the role of miR-1303. After synthesis of nanoparticles carrying miR-1303 and transfection, CCK-8 method and assays were used to evaluate cell growth and apoptosis. The target genes for miR-1303 were predicted using bioinformatics software, and binding of miR-1303 to SNHG16 was evaluated using the dual-luciferase reporter assay. miR-1303 was lowly expressed in RCC cells, with lowest level in A498 (p < 0.05). Overexpressed miR-1303 significantly reduced proliferation ability of RCC cells and induced apoptosis (p < 0.05). Besides, transfection of NP carrying miR-1303 mimic resulted in dramatically decreased migrated cells when reducing the expression of SNHG18 mRNA. The presence of NPs strengthened the inhibitory effect of miR-1303 on RCC. Furthermore, the miR-1303+SNHG16-WT co-transfection group had lower relative luciferase activity compared with miR-1303+SNHG16-MUT co-transfection group (p < 0.05). miR-1303 was down-regulated in RCC and NP delivery of miR-1303 inhibited RCC cell proliferation and differentiation through regulation of SNHG16. These findings suggest miR-1303 may become a potential molecular target for RCC.