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  • Open Access

    ARTICLE

    Overexpression of MicroRNA-216a Suppresses Proliferation, Migration, and Invasion of Glioma Cells by Targeting Leucine-Rich Repeat-Containing G Protein-Coupled Receptor 5

    Junfeng Zhang*1, Kun Xu†1, Lili Shi*, Li Zhang*, Zhaohua Zhao*, Hao Xu*, Fei Liang*, Hongbo Li*, Yan Zhao*, Xi Xu*, Yingfang Tian

    Oncology Research, Vol.25, No.8, pp. 1317-1327, 2017, DOI:10.3727/096504017X14874323871217

    Abstract Increasing studies have suggested that microRNAs (miRNAs) are involved in the development of gliomas. MicroRNA-216a has been reported to be a tumor-associated miRNA in many types of cancer, either as an oncogene or as a tumor suppressor. However, little is known about the function of miR-216a in gliomas. The present study was designed to explore the potential role of miR-216a in gliomas. We found that miR-216a was significantly decreased in glioma tissues and cell lines. Overexpression of miR-216a significantly suppressed the proliferation, migration, and invasion of glioma cells. Leucine-rich repeat-containing G protein-coupled receptor 5 (LGR5) More >

  • Open Access

    ARTICLE

    Fzd2 Contributes to Breast Cancer Cell Mesenchymal-Like Stemness and Drug Resistance

    Ping Yin*, Wei Wang*, Jian Gao, Yu Bai*, Zhuo Wang*, Lei Na*, Yu Sun*, Chenghai Zhao*

    Oncology Research, Vol.28, No.3, pp. 273-284, 2020, DOI:10.3727/096504020X15783052025051

    Abstract Cancer cell stemness is responsible for cancer relapse, distal metastasis, and drug resistance. Here we identified that Frizzled 2 (Fzd2), one member of Wnt receptor Frizzled family, induced human breast cancer (BC) cell stemness via noncanonical Wnt pathways. Fzd2 was overexpressed in human BC tissues, and Fzd2 overexpression was associated with an unfavorable outcome. Fzd2 knockdown (KD) disturbed the mesenchymallike phenotype, migration, and invasion of BC cells. Moreover, Fzd2 KD impaired BC cell mammosphere formation, reduced Lgr5+ BC cell subpopulation, and enhanced sensitivity of BC cells to chemical agents. Mechanistically, Fzd2 modulated and bound with More >

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