Browsing by Subject "miR-330-5p"

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    CircRNF220 plays a pathogenic role to facilitate cell progression of AML in vitro via sponging miR-330-5p to induce upregulation of SOX4
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Zhang, Zewen; Lin, Shujun; Yin, Jun; Yu, Wenjun; Xu, Chengwei
    Background: Circular RNAs (circRNAs) are a specific family of non-coding RNAs (ncRNAs) with important function in disease progression. This research is performed to study circRNA Ring Finger Protein 220 (circRNF220) in acute myeloid leukemia (AML). Methods: CircRNF220, microRNA-330-5p (miR330-5p) and sex-determining region Y-related highmobility group box 4 (SOX4) were measured via quantitative real-time polymerase chain reaction (qRTPCR). 3-(4, 5-dimethylthiazol-2-y1)-2, 5- diphenyl tetrazolium bromide (MTT) and EdU assays were used to assess cell proliferation. Cell cycle and apoptosis were detected using flow cytometry. Cell invasion was determined by transwell assay. Glycolytic metabolism was assessed by glucose consumption and lactate production. The target interaction was implemented via dual-luciferase reporter and RNA pull-down assays. SOX4 protein detection was conducted by western blot. Results: Expression detection identified that circRNF220 was overexpressed in AML. In vitro experiments showed that silence of circRNF220 promoted cell apoptosis but impeded proliferation, cell cycle progression, invasion and glycolytic metabolism in AML cells. Target analysis indicated that circRNF220 directly targeted miR-330-5p, and the effects of sicircRNF220 were abrogated by miR-330-5p inhibitor. Moreover, circRNF220 targeted miR-330-5p to increase the expression of SOX4 and SOX4 promoted cell progression of AML. Conclusion: All these findings revealed that circRNF220 contributed to AML cell development in vitro via upregulating SOX4 expression by targeting miR-330-5p.
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    Circular RNA circ-CD44 regulates chemotherapy resistance by targeting the miR-330-5p/ABCC1 axis in colorectal cancer cells
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2023) Zhao, Shuai; Xu, Fei; Ji, Yiding; Wang, Yuanyuan; Wei, Ming; Zhang, Like
    . Background. Colorectal cancer (CRC) is a common malignant tumor worldwide, ranking fourth for incidence. Recently, circular RNAs (circRNAs) have been demonstrated to play a key role in chemotherapy resistance to CRC treatment. Therefore, the role of circCD44 is investigated in CRC. Methods. The expression levels of circ-CD44, miR330-5p, and ATP binding cassette subfamily C member 1 (ABCC1) were quantified by real-time quantitative polymerase chain reaction (RT-qPCR) assay. The sensitivity of CRC cells to oxaliplatin (OXA) was assessed by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl2H-tetrazol-3-ium bromide (MTT) assay. Colonyforming experiment was performed to measure the colony-forming ability of CRC cells. The apoptosis, migration, and invasion of CRC cells were determined by flow cytometry and transwell assays. A xenograft experiment was established to clarify the functional role of circ-CD44 silencing in vivo. The interactional relationship among circ-CD44, miR-330-5p, and ABCC1 was confirmed by dual-luciferase reporter and RNA immunoprecipitation assays. The protein expression of ABCC1 was quantified by western blot assay. Results. Circ-CD44 was obviously upregulated in OXA-resistant colorectal cancer tissues and cells. Lossof-function experiments revealed that inhibition of circCD44 suppressed proliferation, migration, and invasion while it increased OXA sensitivity and apoptosis in OXA-resistant colorectal cancer cells, which was overturned by suppression of miR-330-5p; besides, silencing of circ-CD44 also slowed the tumor growth in vivo. Additionally, overexpression of miR-330-5p inhibited chemotherapy resistance, proliferation, migration, and invasion while it induced apoptosis by targeting ABCC1. Conclusion. Mechanistically, circ-CD44 functioned as a miRNA sponge for miR-330-5p to upregulate the expression of ABCC1 and regulate chemotherapy resistance in CRC cells