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derlying genes in sheep breeding.Gastric cancer is the third leading cause of cancer-related death worldwide, with relapse and metastasis being major contributors to the mortality. Circular RNAs (circRNAs) have been at the center of several researches and some circRNAs have been indicated to be involved in gastric cancer as sponges. Nevertheless, the mechanism underlying the function of circRNA remains largely unclear. Therefore, this study was conducted with the main objective of screening the associated circRNA in gastric cancer and exploring its mechanism. Expression of hsa_circRNA_0009172 was validated in gastric cancer tissues and cell lines after the correlation between hsa_circRNA_0009172 and prognosis was determined. NSC23766 Moreover, the binding site between miR-485-3p and hsa_circRNA_0009172 or NTRK3 was verified using dual luciferase assay and RNA pull down. Function-gain and -loss experiments were performed for the purpose of detecting the effect of hsa_circRNA_0009172 in vivo and in vitro as well as its mechanism with microRNA (miRNA)-485-3p and NTRK3 in gastric cancer. The hsa_circRNA_0009172 expression was downregulated in gastric cancer tissues and cell lines, indicating a positive association with patient prognosis. Functionally, hsa_circ_0009172 overexpression inhibited proliferative, invasive and migrative potential of gastric cancer cells as well as epithelial-mesenchymal transition (EMT)-related proteins by sponging miR-485-3p to inhibit NTRK3, while miR-485-3p overexpression could reverse the inhibitory effect of hsa_circ_0009172 on gastric cancer. Furthermore, either up-regulation of hsa_circ_0009172 or down-regulation of miR-485-3p led to the suppression of xenograft tumor growth in nude mice. In conclusion, hsa_circ_0009172 serves as a tumor suppressor in gastric cancer by targeting miR-485-3p/NTRK3 axis.Colorectal cancer (CRC) is a prevalent malignancy with high incidence and low 5-year survival. Long non-coding RNAs (lncRNAs), a kind of specific RNA transcript, are increasingly implicated in tumor growth, metastasis, invasion, and prognosis by regulating the tumor microenvironment in extracellular vesicles (EVs). This study aims at investigating the potential effect of lncRNA HLA-F-AS1 on CRC by affecting the profilin 1 (PFN1) expression pattern in the tumor EVs. The expression patterns of HLA-F-AS1 and miR-375 were determined by RT-qPCR in the CRC tissues and cells. CCK-8 and Transwell assays were conducted to detect the cell proliferation and migration, and invasion, respectively. Western blot analysis was performed to measure the expression pattern of the epithelial-mesenchymal transition (EMT) markers. Bioinformatics prediction website and dual-luciferase reporter assay were conducted to verify the interaction between HLA-F-AS1 and miR-375. The CRC-derived EVs were extracted with the expression pattern 1 promotes the expression pattern of PFN1 in CRC-EVs by inhibiting miR-375, thereby polarizing macrophages toward M2 phenotype, and aggravating the tumorigenesis of CRC, eliciting that HLA-F-AS1 may serve as a viable and promising therapeutic strategy for CRC.Increasing evidence proved the abnormal expression of long non-coding RNAs (lncRNAs) in various human malignancies, including oral squamous cell carcinoma (OSCC). Nevertheless, limited explorations concern the role of lncRNA small nucleolar RNA host gene 17 (SNHG17) in OSCC. Herein, SNHG17 was disclosed to be remarkably upregulated in OSCC cell lines and promoted OSCC cell growth. Further mechanistic studies, including DNA/RNA pull down, RIP, ChIP, and luciferase reporter gene assays, were conducted. It was confirmed that Wnt/β-catenin signaling pathway was involved in the SNHG17-mediated OSCC cell growth. Moreover, E74 like ETS transcription factor 1 (ELF1) was identified as the transcription activator of CTNNB1 (β-catenin mRNA) in OSCC. Inspired by competing for endogenous RNAs (ceRNAs) network, we were pleasantly surprised to find that SNHG17 and ELF1 functioned as ceRNAs in OSCC via competitively binding to microRNA-384 (miR-384). By using rescue assays, we revealed that SNHG17 facilitated OSCC cell growth through modulating miR-384/ELF1 axis. Importantly, we certified that ELF1 was indispensable for SNHG17-affected OSCC progression. Collectively, it can be concluded that SNHG17/miR-384/ELF1 axis contributed to OSCC cell growth via promoting CTNNB1 expression, thus activating Wnt/β-catenin signaling pathway.microRNAs (miRNAs) have been revealed to participate in some oral cancers and are proved to be effective. In the present study, we tried to explore the biological function of miR-133a in oral squamous cell carcinoma (OSCC) cells. The relationship that C-terminal-binding proteins 2 (CTBP2) was the putative target gene of miR-133a revealed from bioinformatics analysis was further was further validated by dual-luciferase reporter gene assay. In total, 40 patients with OSCC were enrolled for characterization of miR-133a, CTBP2, and Notch signaling pathway-related gene expression in clinical OSCC tissues. Low expression of miR-133a and high expression of CTBP2, Hes1, Notch-1, and Notch-3 were determined in OSCC tissues. OSCC cell lines were transfected with miR-133a inhibitor, miR-133a mimic, or shRNA targeting CTBP2, in response to which cell proliferation, migration, invasion, cell cycle, and apoptosis were evaluated. Transfection of miR-133a mimic induced apoptosis and inhibited OSCC cell proliferation, migration, and invasion and this was demonstrated to be attributable to decreased CTBP2 expression and suppression of the Notch signaling pathway. Taken together, we concluded that miR-133a acted as a tumor suppressor in OSCC through inhibition of the Notch signaling pathway via binding to CTBP2.The purpose of this study is to determine whether multiparametric non-contrast MR imaging including diffusion-weighted imaging (DWI), arterial spin labeling (ASL), and amide proton transfer (APT) weighted imaging can help differentiate malignant from benign salivary gland lesions. The study population consisted of 42 patients, with 31 benign and 11 malignant salivary gland lesions. All patients were evaluated using DWI, three-dimensional pseudo-continuous ASL, and APT-weighted imaging on 3 T MR imaging before treatment. Apparent diffusion coefficient (ADC), tumor blood flow (TBF), and APT-related signal intensity (APTSI) values within the lesion were compared between the malignant and benign lesions by Mann-Whitney U test. For each parameter, optimal cutoff values were chosen using a threshold criterion that maximized the Youden index for predicting malignant lesions. The performance of ADC, TBF, APTSI, individually and combined, was evaluated in terms of diagnostic ability for malignant lesions. Diagnostic performance was compared by McNemar test.