BackgroundData on the expression of RCC tissues from the GEO database and patient survival data from TCGA were used to explore the prognostic significance of long noncoding RNA SNHG1. SNHG1 has been reported to participate in the development of several cancers, but, the underlying mechanism of SNHG1 in renal cell carcinoma (RCC) has not been reported. The purpose of our study was to investigate the potential function of SNHG1 in RCC.Material/MethodsThe expression of SNHG1 in 40 cases of RCC and adjacent normal tissues and 5 cell lines was detected by qRT-PCR. Cell proliferation, Transwell assay, and Western blotting assay were carried out to investigate the biological function of SNHG1. A rescue experiment was performed to verify that miR-137 can partly impede the effect of SNHG1 on renal cancer cells.ResultsSNHG1 was identified to be overexpressed in RCC tissues and RCC cell lines. High levels of SNHG1 were correlated with poor prognosis of RCC patients. Knockdown of SNHG1 suppressed the proliferation, invasion, and EMT capacity in RCC. Moreover, miR-137 abrogated the effect of SNHG1 on RCC.ConclusionsSNHG1 is significantly upregulated in RCC and renal cancer cell lines. Overexpression of SNHG1 participates in RCC tumorigenesis by regulating miR-137.

An increasing body of evidence has indicated that microRNAs (miRNAs/miRs) may play an important role in tumourigenesis and tumour progression. Recent studies have demonstrated that miR-320a is aberrantly expressed in a variety of different types of human cancer. The results of the present study confirmed that the expression of miR-320a was decreased in clinical specimens and cell lines. Expression of miR-320a inhibited the growth and invasive ability of ACHN and Caki-1 cells. Bioinformatics analysis and a luciferase reporter assay demonstrated that forkhead box protein M1 (FoxM1) was directly regulated by miR-320a. Rescue experiments in vitro revealed that the upregulation of FoxM1 antagonized the miR-320a-mediated malignant phenotype in renal cancer. Furthermore, experiments employing a xenograft mouse model revealed that the upregulation of miR-320a inhibited the proliferation of renal cancer cells in nude mice when FoxM1 protein expression was reduced. Collectively, the present study demonstrated a novel molecular interaction regulated by miR-320a, which may provide a novel insight into the treatments for renal cancer.

Artificial intelligence has been widely applied to e-commerce and the online business service field. However, few studies have focused on studying the differences in the effects of types of customer service on customer purchase intentions. Based on service encounter theory and superposition theory, we designed two shopping experiments to capture customers’ thoughts and feelings, in order to explore the differences in the effects of three different types of online customer service (AI customer service, manual customer service, and human–machine collaboration customer service) on customer purchase intention, and analyses the superposition effect of human–machine collaboration customer service. The results show that the consumer’s perceived service quality positively influences the customer’s purchase intention, and plays a mediating role in the effect of different types of online customer service on customer purchase intention; the product type plays a moderating role in the relationship between online customer service and customer purchase intention, and human–machine collaboration customer service has a superposition effect. This study helped to deepen the understanding of AI developers and e-commerce platforms regarding the application of AI in online business service, and provides reference suggestions for the formulation of more perfect business service strategies.

Renal fibrosis is a common pathological feature of chronic kidney disease (CKD) patients who progress to end-stage renal disease (ESRD). With the increasing incidence of CKD, it is of importance to develop effective therapies that blunt development of renal fibrosis. FFNT25 is a newly developed molecular compound that could be used to prevent fibrosis. In this study, we administered FFNT25 to rats following unilateral ureteral obstruction (UUO) to investigate its anti-fibrosis mechanism. Thirty-two Sprague-Dawley rats were randomly divided into four groups: (1) control (normal rats), (2) sham-operated, (3) UUO-operated + vehicle, and (4) UUO-operated + FFNT25. Two weeks after UUO, the rats were gavaged with either FFNT25 (20.6 mg/kg/day) or vehicle for two weeks. Serum, urine, and kidney samples were collected at the end of the study. FFNT25 reduced levels of renal fibrosis and decreased mRNA and protein levels of extracellular matrix (ECM) markers α-smooth muscle actin (α-SMA) and plasminogen activator inhibitor-1 (PAI-1) following UUO compared to vehicle treatment ( n = 8, p <.05). The current results indicate that FFNT25 can affect both the production and degradation of collagen fibers to reduce fibrosis.

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