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  • Open Access

    ARTICLE

    Knockdown of Urothelial Carcinoma-Associated 1 Suppressed Cell Growth and Migration Through Regulating miR-301a and CXCR4 in Osteosarcoma MHCC97 Cells

    Genglong Zhu*, Xialei Liu*, Yonghui Su, Fangen Kong, Xiaopeng Hong*, Zhidong Lin

    Oncology Research, Vol.27, No.1, pp. 55-64, 2019, DOI:10.3727/096504018X15201143705855

    Abstract Liver cancer is one of the most common malignancies in the world and a leading cause of cancer-related mortality. Accumulating evidence has highlighted the critical role of long noncoding RNAs (lncRNAs) in various cancers. The present study aimed to explore the role of lncRNA urothelial carcinoma-associated 1 (UCA1) in cell growth and migration in MHCC97 cells and its underlying mechanism. First, we assessed the expression of UCA1 in MHCC97 and three other cell lines by RT-qPCR. Then the expression of UCA1, miR-301a, and CXCR4 in MHCC97 cells was altered by transient transfection. The effects of UCA1 and miR-301 on cell… More >

  • Open Access

    ERRATUM

    Long Noncoding RNA UCA1 Targets miR-122 to Promote Proliferation, Migration, and Invasion of Glioma Cells

    Yang Sun*1, Jun-Gong Jin*1, Wei-Yang Mi, Hao-Wu*, Shi-Rong Zhang, Qiang Meng*, Shi-Tao Zhang

    Oncology Research, Vol.28, No.6, pp. 683-684, 2020, DOI:10.3727/096504021X16137463165433

    Abstract Glioma is the most common and lethal malignant intracranial tumor. Long noncoding RNAs (lncRNAs) have been identified as pivotal regulators in the tumorigenesis of glioma. However, the role of lncRNA urothelial carcinoma-associated 1 (UCA1) in glioma genesis is still unknown. The purpose of this study was to investigate the underlying function of UCA1 on glioma genesis. The results demonstrated that UCA1 was upregulated in glioma tissue and indicated a poor prognosis. UCA1 knockdown induced by si-UCA1 significantly suppressed the proliferative, migrative, and invasive activities of glioma cell lines (U87 and U251). Bioinformatics analysis and luciferase reporter assay verified the complementary… More >

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