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  • Open Access

    ARTICLE

    miR-200b-3p accelerates progression of pituitary adenomas by negatively regulating expression of RECK

    XIAOXI WANG1, YANFEI JIA2, QIANG LI2, QIANG YANG2, YINGFENG LIU1, BEIFENG WEI1, XIANG NIU1, YINJIE ZHANG1, XIAODONG LUO2, ZIYU ZHAO1,*, PENG WANG1,*

    Oncology Research, Vol.32, No.5, pp. 933-941, 2024, DOI:10.32604/or.2023.042581

    Abstract MicroRNA (miR)-200b-3p has been associated with many tumors, but its involvement in pituitary adenoma is unclear. This study investigated the molecular mechanism underlying miR-200b-3p regulation in pituitary adenomas to provide a theoretical basis for treatment. Bioinformatics was used to analyze pituitary adenoma-related genes and screen new targets related to RECK and miRNA. As well, the relationship between miR-200b-3p and RECK protein was verified using a double-luciferase reporter gene assay. The expression of miR-200b-3p in clinical samples was analyzed by in situ hybridization. Transfection of the miR-200b-3p inhibitor and small interfering-RECK (si-RECK) was verified by qPCR. GH3 cell viability and proliferation… More >

  • Open Access

    ARTICLE

    RPSAP52 lncRNA Inhibits p21Waf1/CIP Expression by Interacting With the RNA Binding Protein HuR

    Daniela D’Angelo*, Claudio Arra, Alfredo Fusco*

    Oncology Research, Vol.28, No.2, pp. 191-201, 2020, DOI:10.3727/096504019X15761465603129

    Abstract Long noncoding RNAs have been recently demonstrated to have an important role in fundamental biological processes, and their deregulated expression has been found in several human neoplasias. Our group has recently reported a drastic overexpression of the long noncoding RNA (lncRNA) RPSAP52 (ribosomal protein SA pseudogene 52) in pituitary adenomas. We have shown that this lncRNA increased cell proliferation by upregulating the expression of the chromatinic proteins HMGA1 and HMGA2, functioning as a competing endogenous RNA (ceRNA) through competitively binding to microRNA-15a (miR-15a), miR-15b, and miR-16. The aim of this work was to identify further mechanisms by which RPSAP52 overexpression… More >

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