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Title:
Hsa_circ_0011292 regulates paclitaxel resistance partially through regulating CDCA4 expression by serving as a miR-3619-5p sponge in non-small cell lung cancer | Molecular & Cellular Toxicology
Description:
Background Circular RNA hsa_circ_0011292 (circ_0011292) participates in NSCLC resistance to paclitaxel (PTX). Here, we further clarify the mechanism of circ_0011292 regulating non-small cell lung cancer (NSCLC) resistance to PTX. Objectives Expression patterns of circ_0011292, microRNA (miR)-3619-5p, and CDCA4 mRNA were verified by qRT-PCR. The IC50 (half-maximal inhibitory concentration) value, proliferation, migration, invasion, and apoptosis were analyzed by MTT, transwell, and flow cytometry assays. Protein levels were measured by western blotting (WB). The regulation mechanism of circ_0011292 was analyzed by bioinformatics analysis, dual-luciferase reporter, and/or RNA pull-down assays. Results Circ_0011292 was highly expressed in PTX-resistant NSCLC. Functionally, circ_0011292 inhibition lowered cell IC50 value, induced cell apoptosis, and repressed cell proliferation, migration, and invasion in PTX-resistant NSCLC cells in vitro. Mechanically, circ_0011292 acted as a decoy for miR-3619-5p, which targeted CDCA4 in PTX-resistant NSCLC cells. Both miR-3619-5p inhibitor and CDCA4 overexpression overturned circ_0011292 inhibition-mediated influence on PTX sensitivity and malignant behaviors of PTX-resistant NSCLC cells. Importantly, circ_0011292 adsorbed miR-3619-5p to regulate CDCA4 expression. Conclusions Circ_0011292 facilitates PTX resistance in NSCLC partially through the miR-3619-5p/CDCA4 pathway, highlighting a new mechanism responsible for PTX resistance in NSCLC.
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pubmed, article, cancer, google, scholar, cell, cas, lung, central, resistance, nsclc, circ, zhang, nonsmall, mirp, expression, cdca, chen, liu, wang, progression, data, paclitaxel, regulating, cui, ptx, cells, axis, privacy, cookies, content, hsacirc, bao, luan, proliferation, access, promotes, rev, med, sci, mol, kunming, analysis, consent, information, publish, search, yumin, mechanism, regulation,
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regulating mir-379-5p/trim65 axis wnt/Ξ²-catenin signaling due downregulating exosomal mir-15a-5p mirna-153-3p promotes gefitinib-sensitivity month download article/chapter small-cell lung cancer mir-150-5p/glut-1 axis mir-3619-5p/tbl1xr1 axis neat1 mediates paclitaxel-resistance cutaneous squamous-cell carcinoma mir-3619-5p/cdca4 pathway circ_0011292 adsorbed mir-3619-5p half-maximal inhibitory concentration akt/mtor signalling pathway ptx-resistant nsclc cells mir-3619-5p hampers proliferation directly targeting Ξ²-catenin Ξ²-catenin-mediated tumor suppressor genes full article pdf regulating cdca4 expression circular rnas yue cui declares mir-3619-5p inhibitor targeting mir-182-5p sponging mir-3619-5p regulate cdca4 expression privacy choices/manage cookies cisplatin resistance yumin luan declares mir-3619-5p sponge ptx-resistant nsclc circrna-microrna code drug target 27 article bao cell division cycle promotes metastatic colonization jun oncogene expression inhibiting atg5 expression global cancer incidence cancer biother radiopharm repressed cell proliferation small cell lung cancer paclitaxel resistance open biol 9 nsclc partially induced cell apoptosis pan-cancer analysis article log
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headline:Hsa_circ_0011292 regulates paclitaxel resistance partially through regulating CDCA4 expression by serving as a miR-3619-5p sponge in non-small cell lung cancer
description:Circular RNA hsa_circ_0011292 (circ_0011292) participates in NSCLC resistance to paclitaxel (PTX). Here, we further clarify the mechanism of circ_0011292 regulating non-small cell lung cancer (NSCLC) resistance to PTX. Expression patterns of circ_0011292, microRNA (miR)-3619-5p, and CDCA4 mRNA were verified by qRT-PCR. The IC50 (half-maximal inhibitory concentration) value, proliferation, migration, invasion, and apoptosis were analyzed by MTT, transwell, and flow cytometry assays. Protein levels were measured by western blotting (WB). The regulation mechanism of circ_0011292 was analyzed by bioinformatics analysis, dual-luciferase reporter, and/or RNA pull-down assays. Circ_0011292 was highly expressed in PTX-resistant NSCLC. Functionally, circ_0011292 inhibition lowered cell IC50 value, induced cell apoptosis, and repressed cell proliferation, migration, and invasion in PTX-resistant NSCLC cells in vitro. Mechanically, circ_0011292 acted as a decoy for miR-3619-5p, which targeted CDCA4 in PTX-resistant NSCLC cells. Both miR-3619-5p inhibitor and CDCA4 overexpression overturned circ_0011292 inhibition-mediated influence on PTX sensitivity and malignant behaviors of PTX-resistant NSCLC cells. Importantly, circ_0011292 adsorbed miR-3619-5p to regulate CDCA4 expression. Circ_0011292 facilitates PTX resistance in NSCLC partially through the miR-3619-5p/CDCA4 pathway, highlighting a new mechanism responsible for PTX resistance in NSCLC.
datePublished:2022-07-22T00:00:00Z
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headline:Hsa_circ_0011292 regulates paclitaxel resistance partially through regulating CDCA4 expression by serving as a miR-3619-5p sponge in non-small cell lung cancer
description:Circular RNA hsa_circ_0011292 (circ_0011292) participates in NSCLC resistance to paclitaxel (PTX). Here, we further clarify the mechanism of circ_0011292 regulating non-small cell lung cancer (NSCLC) resistance to PTX. Expression patterns of circ_0011292, microRNA (miR)-3619-5p, and CDCA4 mRNA were verified by qRT-PCR. The IC50 (half-maximal inhibitory concentration) value, proliferation, migration, invasion, and apoptosis were analyzed by MTT, transwell, and flow cytometry assays. Protein levels were measured by western blotting (WB). The regulation mechanism of circ_0011292 was analyzed by bioinformatics analysis, dual-luciferase reporter, and/or RNA pull-down assays. Circ_0011292 was highly expressed in PTX-resistant NSCLC. Functionally, circ_0011292 inhibition lowered cell IC50 value, induced cell apoptosis, and repressed cell proliferation, migration, and invasion in PTX-resistant NSCLC cells in vitro. Mechanically, circ_0011292 acted as a decoy for miR-3619-5p, which targeted CDCA4 in PTX-resistant NSCLC cells. Both miR-3619-5p inhibitor and CDCA4 overexpression overturned circ_0011292 inhibition-mediated influence on PTX sensitivity and malignant behaviors of PTX-resistant NSCLC cells. Importantly, circ_0011292 adsorbed miR-3619-5p to regulate CDCA4 expression. Circ_0011292 facilitates PTX resistance in NSCLC partially through the miR-3619-5p/CDCA4 pathway, highlighting a new mechanism responsible for PTX resistance in NSCLC.
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