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Circular RNA (circRNA) is a class of endogenous non-coding RNA, a type of single-stranded covalently closed RNA molecule formed by alternative splicing of exons or introns. Previous studies have demonstrated that circRNA participates in modulating biological processes such as cell proliferation, differentiation and apoptosis, and plays key roles in tumor occurrence and development. CircRNA nuclear receptor interacting protein 1 (circ_NRIP1), a form of circRNA, is abnormally expressed in certain human tumor types. It is present at a higher abundance compared with cognate linear transcripts and can regulate malignant biological behaviors such as tumor proliferation, invasion and migration, revealing a currently unexplored frontier in cancer progression. The present review presents a pattern of circ_NRIP1 expression in various malignant tumor types and highlights its significance in cancer development, in addition to its potential as a disease indicator or future therapeutic agent.

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Circular RNAs (circRNAs), a novel type of covalently closed non-coding RNAs, are widely expressed in eukaryotes and viruses. Accumulating evidence has shown that circRNAs play key roles in the pathophysiological changes process of human diseases and can affect cancer development and progression through regulating target genes expression, linear RNA transcription and protein generation. Recent studies had found that circRNA-UBAP2 (ubiquitin binding associated protein 2) was aberrantly expressed in various human tumors and could affect tumor cells proliferation, migration, invasion, cell cycle, anti-apoptosis, radioresistance, chemoresistance and other malignant biological behavioral progress. Mechanistic studies further revealed that circUBAP2 could affect the occurrence and development of human tumors through multiple different molecular regulatory pathways in vivo and in vitro. In addition, the abnormal expression of circUBAP2 was significantly correlated with the clinicopathological characteristics of malignant tumors and had potential value as biomarkers for the diagnosis and prognosis evaluation of cancer patients, which deserved further study. This review had summarized and discussed the oncogenic roles and clinical performances of circUBAP2 in various human malignancies with a focus on biological functions and molecular mechanisms, which could help to elevate the understanding to the roles of circRNAs and continue subsequent studies on circUBAP2.

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CircRNAs have been the focus of research in recent years. They are differentially expressed in various human tumors and can regulate oncogenes and tumor suppressor genes expression through various mechanisms. The diversity, stability, evolutionary conservatism and cell- or tissue-specific expression patterns of circRNAs also endow them with important regulatory roles in promoting or inhibiting tumor cells malignant biological behaviors progression. More interestingly, emerging studies also found that circRNAs can regulate not only other genes expression, but also their parental gene expression and thus influence tumors development. Apart from some conventional features, circRNAs have a certain specificity in the regulation of parental gene expression, with a higher proportion affecting parental gene transcription and easier translation into protein to regulate parental gene expression. CircRNAs are generally thought to be unable to produce proteins and therefore the protein-coding ability exhibited by circRNAs in regulating parental gene expression is unique and indicates that the regulatory effects of parental gene expression by circRNAs are not only a competitive binding relationship, but also a more complex molecular relationship between circRNAs and parental gene, which deserves further study. This review summarizes the molecular mechanisms of circRNAs regulating parental gene expression and their biological roles in tumorigenesis and development, aiming to provide new ideas for the clinical application of circRNAs in tumor-targeted therapy.

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Long noncoding RNAs (lncRNAs) have been reported to exhibit a crucial regulatory role in tumor progression, including cholangiocarcinoma (CCA). As a promising lncRNA, proteasome 20S subunit alpha 3 antisense RNA 1 (PSMA3-AS1) is involved in development of various tumors. However, the role and function of PSMA3-AS1 in CCA remain unclear. The aim of this study is to examine the expression, function, mechanism, and clinical significance of PSMA3-AS1 in CCA development. By TCGA database analysis, we found that PSMA3-AS1 was overexpressed in CCA. Consistent with the TCGA analysis, PSMA3-AS1 was significantly overexpressed in CCA tissues and cells by RT-qPCR. Upregulated PSMA3-AS1 was related to lymph node invasion, advanced TNM stage and poor survival, and was an independent risk factor of prognosis for CCA patients. Functionally, CCK-8, EdU and colony formation assays confirmed that upregulated PSMA3-AS1 promoted CCA cell proliferation, whereas downregulated PSMA3-AS1 inhibited proliferation. This result was further confirmed by subcutaneous tumor formation in nude mice. Wound healing and transwell assays confirmed that increased PSMA3-AS1 promoted CCA cell migration and invasion, whereas decreased PSMA3-AS1 inhibited these biological phenotypes. In addition, PSMA3-AS1 promoted the EMT process of CCA by downregulating E-cadherin and upregulating N-cadherin and vimentin. Mechanistically, transcription factor PAX5 bound to the promoter region of PSMA3-AS1 and promoted its transcription. Simultaneously, PSMA3-AS1 primarily localized in the cytoplasm could competitively bind miR-376a-3p to upregulate LAMC1, thereby accelerating CCA progression. This study uncovers that PSMA3-AS1 functions as a cancer-promoting gene in CCA, and PAX5/PSMA3-AS1/miR-376a-3p/LAMC1 axis plays a vital role in CCA development.

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Cholangiocarcinoma is a highly aggressive malignant tumor, and its incidence is increasing all over the world. More and more evidences show that the aberrant expression of circular RNAs play important roles in tumorigenesis and progression. Current studies on the expression and function of circRNAs in cholangiocarcinoma are scarce. In this study, circ-ZNF609 was discovered as a novel circRNA highly expressed in cholangiocarcinoma for the first time. The circ-ZNF609 expression is connected with the advanced TNM stage, lymphatic invasion and survival time in cholangiocarcinoma patients, and can be used as an independent prognostic factor for the patients. Circ-ZNF609 can promote the cholangiocarcinoma cells proliferation, migration and invasion in vitro, it can also catalyze the xenograft growth in vivo. The promoting effect of circ-ZNF609 on cholangiocarcinoma is achieved via oncogene LRRC1 up-regulation through targeting miR-432-5p by endogenous competitive RNA mechanism. In addition, transcription factor YY1 can bind to the promoter of ZNF609 to further facilitate the transcription of circ-ZNF609. RNA binding protein eIF4A3 can bind to the pre-mRNA of circ-ZNF609 which promotes the circ-ZNF609 circular formation. Overall, YY1/eIF4A3/circ-ZNF609/miR-432-5p/LRRC1 have a significant role in progression of cholangiocarcinoma, and circ-ZNF609 is expected to become a novel biomarker for targeted therapy and prognosis evaluation of cholangiocarcinoma.

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BACKGROUND: Identification of functional genes or biomarkers may be helpful for developing new treatment strategies in lung adenocarcinoma (LUAD). The centromere protein K (CENPK) gene has been discovered to be overexpressed and could influence tumor progression in several tumor types. However, its role in LUAD has never been revealed. OBJECTIVES: The purpose of the current study was to detect the effects of CENPK and its mechanisms in the progression of LUAD. MATERIAL AND METHODS: Data from The Cancer Genome Atlas (TCGA) and Oncomine databases was used to analyze the expression of CENPK. The relationship between CENPK expression and the prognosis of LUAD was investigated using Kaplan-Meier and Cox regression analyses. The cell viability was monitored with Cell Counting Kit-8 (CCK-8) and colony forming assays, while migration and invasion were analyzed with a transwell assay. The effect of CENPK on the expression of epithelial-mesenchymal transition (EMT) markers were estimated using western blotting. RESULTS: CENPK was significantly overexpressed in LUAD tissues and cells (p < 0.01). The overall survival rate in the low CENPK expression group was significantly higher than in the high CENPK expression group (p = 0.003). Furthermore, the overexpression of CENPK facilitated cell viability, migration and invasion of tumor cells, while knockdown of CENPK prevented these behaviors (p < 0.01). Moreover, upregulation of CENPK decreased the expression of E-cadherin and enhanced the expression of N-cadherin, vimentin and Snail in LUAD cells (p < 0.01). Conversely, knockdown of CENPK resulted in the opposite trend (p < 0.01). CONCLUSIONS: CENPK was upregulated in LUAD tissues and cells, and the enhancement of CENPK promoted the viability, migration, invasion, and EMT of LUAD cells.

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BACKGROUND: Cisplatin is an extensively used chemotherapy agent for lung cancer, but its drug resistance serves as a huge obstacle for chemotherapy failure of lung cancer patients. Hence, researchers aimed to determine role of sirtuin 3 (SIRT3) considering its action in cisplatin resistance of lung cancer. METHODS: The expression patterns of SIRT3, FOXO3, and CDT1 were determined using RT-qPCR and Immunoblotting in lung cancer. Immunofluorescence and Co-IP were adopted to detect co-localization and interaction of FOXO3 and CDT1. Loss- and gain-function assays were conducted to determine roles of SIRT3, FOXO3, and CDT1 in resulting pathological changes, while biological behavior of cells was determined using a combination of CCK-8, flow cytometry, colony formation, and Transwell assays. The effects of SIRT3 and CDT1 were determined in the nude mice xenografted with the tumor. The proliferation-, angiogenesis-, and apoptosis-associated factors levels were determined using Immunoblotting. RESULTS: SIRT3, FOXO3, and CDT1 expression was suppressed in the lung cancer tissues and cells. FOXO3 positively regulates the CDT1 expression pattern and SIRT3 elevation inhibits FOXO3 at the acetylated level, thus, elevating FOXO3 expression. The elevation of SIRT3, FOXO3, or CDT1 inhibited cell cisplatin resistance of lung cancer cells as well as inhibited viability, proliferation, and invasion in vitro. In vivo experiments, SIRT3 depletion elevated Ki-67 and VEGFA levels, but downregulated cleaved caspase 3 level. CONCLUSION: Collectively, overexpressed SIRT3 elevates expression of FOXO3a/CDT1 axis, thus, contributing to enhanced sensitivity of lung cancer cells.

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CircRNAs (circular RNAs) are single-stranded RNAs that form covalently closed loops and function as important regulatory elements of the genome through multiple mechanisms. Increasing evidence had indicated that circRNAs, which might serve as either oncogenes or tumor suppressors, played vital roles in the pathophysiology of human diseases, especially in tumorigenesis and progression. CircRNA-ZFR (circular RNA zinc finger RNA binding protein) is a circular RNA that had attracted much attention in recent years. It has been found that circRNA-ZFR was abnormally expressed in a variety of malignant tumors, and its dysregulated expression was closely related to tumor stage, cancer metastasis and patients' prognosis. Recent studies had shown that aberrantly expressed circRNA-ZFR could regulate the malignant biological behaviors of tumors through various mechanisms; further exploration of circRNA-ZFR expression in tumors and its regulation on malignant biological behaviors such as tumor proliferation, invasion and drug resistance will provide new ideas for clinical tumors diagnosis and treatment.

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Increasing evidences suggest that insufficient radiofrequency ablation (IRFA) can paradoxically promote tumor invasion and metastatic processes, whereas the effects of moderate hyperthermia on cancer progression are not well illustrated. Our study found that IRFA can increase the in vitro migration, invasion, and epithelial-mesenchymal transition (EMT) of hepatocellular carcinoma (HCC) cells via induction of Snail, a master regulator of EMT events. Among measured miRNAs, IRFA can decrease the expression of miR-148a-5p in HCC cells. Whereas overexpression of miR-148a-5p can reverse IRFA-induced migration of HCC cells and upregulation of Snail, mechanistically overexpression of miR-148a-5p can directly target and decrease the expression of protein kinase ATM (ataxia telangiectasia mutated), which can increase protein stability of Snail. Collectively, our data suggest that IRFA can regulate the miR-148a-5p/ATM/Snail axis to trigger migration of HCC cells.

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OBJECTIVE: To evaluate a method of ultrasound biometry in silicone oil-filled eye and its clinical results. METHODS: This was a series case study. According to the principle of measuring a distance with ultrasound, we compared the measured distance between a space filed with balanced salt solution and silicone oil at same height, to calculate a conversion factor (0.674) between them. A formula for corrective axial length in silicone oil-filled eye was established. The formula = ab + 0.674 x bc (a, b and c standing for the apex of the cornea, the posterior pole of the lens or the center of the capsular membrane and the anterior surface of the macular, respectively). The axial lengths of 150 silicone oil-filled eyes in 150 cases were then measured before and after silicone oil removal with Vivid 7 Dimension ultrasound. According to the axial length, they were divided into two groups, namely group 1 (the length < 25 mm) and group 2 (the length > or = 25 mm). In 76/150 eyes, before combined silicone oil removal and intraocular lens (IOL) implantation, the SRKT formula was used for intraocular lens calculation; the post-operative actual refraction was compared with the pre-operative predicted refraction and statistics analysis was made. RESULTS: The retinal condition of 150 silicone oil-filled eyes in 150 cases after 3 months' follow-up was stable after surgery. The results of the biometry were as follows. In the first group, the mean corrective axial lengths of 111 silicone oil-filled eyes before silicone oil removal was (22.77 +/- 1.00) mm (ranging from 21.10 to 24.90 mm); the mean axial lengths after silicone oil removal was (22.76 +/- 0.99) mm (ranging from 21.00 to 24.70 mm). The difference between them was not statistically significant (t = 0.518, P > 0.05). The vitreous cavity depth before and after silicone oil removal was (26.57 +/- 2.14) mm and (17.90 +/- 1.38) mm, respectively. The ratio of the latter to the former was 0.673 78. In the second group, the mean corrective axial lengths of 39 silicone oil-filled eyes before silicone oil removal was (26.52 +/- 1.31) mm (ranging from 25.00 to 30.58 mm); the mean axial lengths after silicone oil removal was (26.53 +/- 1.29) mm (ranging from 25.00 to 30.59 mm). The difference between them was not statistically significant (t = 0.109, P > 0.05). The vitreous cavity depth before and after silicone oil removal was (32.01 +/- 2.90) mm and (21.57 +/- 2.04) mm, respectively. The ratio of the latter to the former was 0.673 95. In 76 eyes with IOL, the post-operative actual refraction after at least 3 months follow-up was compared with the pre-operative predicted refraction (-1.50 DS) in both groups. The differences between them were not statistically significant (t(1) = 0.253, P(1) > 0.05; t(2) = 0.209, P(2) > 0.05) in each group. CONCLUSION: Ultrasound biometry in silicone oil-filled eye is accurate and simple, and has good results in clinical measurement.

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