Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.27.1 (RNase)
 16,360 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ribonucleases are enzymes that destroy RNA, play an important role in protein synthesis, epigenetic regulation of genetic activity, cell proliferation and apoptosis. Ribonucleases are important antimicrobial, antiviral and immune defense factors. Despite the same biochemical properties, they exhibit unequal, sometimes opposite biological effects. While mostly ribonucleases inhibit cell proliferation, induce apoptosis and inhibit the growth of tumors, some ribonucleases stimulate vascular growth, proliferation and tumor development. RNase inhibitors have an opposite effect. The correct use of these features of RNases can provide additional opportunities for the development of a strategy of targeted influence on tumor growth.
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PMID:The dual role of ribonucleases in tumor-host relationship. 3156 37

Oral squamous cell carcinoma (OSCC) is one of the most common malignancies and has a poor prognosis. Circular RNA (circRNA) has been increasingly recognized as a crucial contributor to carcinogenesis. circRNA_0000140 has been aberrantly expressed in OSCC, but its role in tumor growth and metastasis remains largely unclear. Sanger sequencing, actinomycin D, and RNase R treatments were used to confirm head-to-tail junction sequences and the stability of circ_0000140. In vitro cell activities, including proliferation, migration, invasion, and apoptosis, were determined by colony formation, transwell, and flow cytometry assays. The expression levels of circ_0000140, Hippo signaling pathway, and serial epithelial-mesenchymal transition (EMT) markers were measured by quantitative real-time PCR, western blotting, immunofluorescence, and immunohistochemistry. Dual luciferase reporter assays and Argonaute 2-RNA immunoprecipitation assays were performed to explore the interplay among circ_0000140, miR-31, and LATS2. Subcutaneous tumor growth was observed in nude mice, in which in vivo metastasis was observed following tail vein injection of OSCC cells. circ_0000140 is derived from exons 7 to 10 of the KIAA0907 gene. It was down-regulated in OSCC tissues and cell lines, and correlated negatively with poor prognostic outcomes in OSCC patients. Gain-of-function experiments demonstrated that circ_0000140 enhancement suppressed cell proliferation, migration, and invasion, and facilitated cell apoptosis in vitro. In xenograft mouse models, overexpression of circ_0000140 was able to repress tumor growth and lung metastasis. Furthermore, mechanistic studies showed that circ_0000140 could bind with miR-31 and up-regulate its target gene LATS2, thus affecting OSCC cellular EMT. Our findings demonstrated the roles of circ_0000140 in OSCC tumorigenesis as well as in metastasis, and circ_0000140 exerts its tumor-suppressing effect through miR-31/LATS2 axis of Hippo signaling pathway in OSCC.
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PMID:circRNA_0000140 suppresses oral squamous cell carcinoma growth and metastasis by targeting miR-31 to inhibit Hippo signaling pathway. 3204 42

Background: Circular RNAs (circRNAs) are crucial regulators in human cancers, including nonsmall cell lung cancer (NSCLC). In this study, we aim to explore the biological functions and molecular mechanisms of circ_0074027 in NSCLC. Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to determine the expression of circ_0074027, paired like homeodomain 1 (PITX1) mRNA, microRNA-335-5p (miR-335-5p), and cullin 4B (CUL4B) mRNA. The feature of circ_0074027 was analyzed by RNase R digestion assay. Flow cytometry analysis was adopted to analyze cell cycle and cell apoptosis. Cell counting kit-8 (CCK-8) assay and colony formation assay were performed to assess cell proliferation. Western blot assay was conducted to measure protein levels. Dual-luciferase reporter and RNA pull-down assays were carried out to verify the relationships among circ_0074027, miR-335-5p, and CUL4B. The murine xenograft model was established to investigate the role of circ_0074027 in vivo. Results: High expression of circ_0074027 was found in NSCLC tissues and cells. Circ_0074027 knockdown suppressed cell viability, cell cycle process, and colony formation and promoted apoptosis in NSCLC cells in vitro and inhibited tumor growth in vivo. Circ_0074027 acted as a sponge of miR-335-5p. The effect of circ_0074027 knockdown on NSCLC progression was weakened by miR-335-5p inhibition. Moreover, CUL4B was a target gene of miR-335-5p. CUL4B overexpression reversed the inhibitory effects on cell viability, cell cycle process, and colony formation and the promotional effect on cell apoptosis caused by miR-335-5p in NSCLC. Conclusion: Circ_0074027 facilitated NSCLC cell progression through regulating miR-335-5p/CUL4B axis.
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PMID:Circ_0074027 Contributes to Nonsmall Cell Lung Cancer Progression by Upregulating CUL4B Expression Through miR-335-5p. 3258 May 76

Accumulating evidences indicate that circular RNAs (circRNAs), a subclass of noncoding RNAs, play important role in regulating gene expression in eukaryotes. Hsa_circ_0046263 (circ-0046263) was found aberrantly expressed in nasopharyngeal carcinoma (NPC), but its role in tumor growth and metastasis remains largely unclear. Sanger sequencing, RNase R assay, and nucleic acid electrophoresis were conducted to verify the identification of circ-0046263. Nuclear separation and fluorescence in situ hybridization (FISH) assays were used to determine the localization of circ-004263. Dual luciferase reporter and RNA immunoprecipitation (RIP) were employed to confirm the binding of circ-0046263 with miR-133a-5p. Colony formation, proliferation, wound healing, transwell, western blot, and in vivo tumor growth and metastasis assays were performed to assess the roles of circ-0046263, miR-133a-5p, IGFBP3 and their interactions in NPC cells. Circ-0046263 was upregulated in both NPC cell lines and tissues. The in vitro functional studies revealed that knockdown of circ-0046263 inhibited the proliferation, invasion, and migration of NPC cells, whereas its overexpression produced the opposite result. In vivo experiments indicated that knockdown or overexpression of circ-0046263 attenuated or promoted tumor growth and metastasis, respectively. Mechanistically, circ-0046263 could act as a miRNA sponge to absorb miR-133a-5p and upregulate the expression of miRNA downstream target IGFBP3. In addition, miR-133a-5p inhibition or IGFBP3 overexpression could rescue the malignant behavior induced by circ-0046263 silencing. Finally, circ-0046263 plays a tumor-promoting role in NPC to enhance malignant behavior through the miR-133a-5p/IGFBP3 axis, which could be a potential target for NPC therapy.
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PMID:Hsa_circ_0046263 functions as a ceRNA to promote nasopharyngeal carcinoma progression by upregulating IGFBP3. 3270 44


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