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  • Open Access

    ARTICLE

    miR-181a Inhibits Cervical Cancer Development via Downregulating GRP78

    Chengyan Luo, Jiangnan Qiu

    Oncology Research, Vol.25, No.8, pp. 1341-1348, 2017, DOI:10.3727/096504017X14867268787969

    Abstract Cervical cancer is among the most common cancers inflicting women worldwide. Understanding the pathological mechanisms of cervical cancer development is critical for identifying novel targets for cervical cancer treatment. MicroRNAs (miRs) have various roles in regulating cancer development. In this study, we investigated the potential role of miR-181a and its target in regulating cervical cancer development and chemotherapy resistance. The expression of miR-181a was evaluated and modulated in several human cervical cancer cell lines. The role of miR-181a in regulating cervical cancer growth and chemotherapy sensitivity was investigated in cell culture models and mouse tumor… More >

  • Open Access

    ARTICLE

    Triptolide Inhibits Proliferation and Migration of Human Neuroblastoma SH-SY5Y Cells by Upregulating MicroRNA-181a

    Jian Jiang*, Xuewen Song, Jing Yang*, Ke Lei*, Yongan Ni*, Fei Zhou, Lirong Sun*

    Oncology Research, Vol.26, No.8, pp. 1235-1243, 2018, DOI:10.3727/096504018X15179661552702

    Abstract Neuroblastoma is the primary cause of cancer-related death for children 1 to 5 years of age. New therapeutic strategies and medicines are urgently needed. This study aimed to investigate the effects of triptolide (TPL), the major active component purified from Tripterygium wilfordii Hook F, on neuroblastoma SH-SY5Y cell proliferation, migration, and apoptosis, as well as underlying potential mechanisms. We found that TPL inhibited SH-SY5Y cell viability, proliferation, and migration, but induced cell apoptosis. The expression of matrix metalloproteinase-2 (MMP-2) and MMP-9 after TPL treatment in SH-SY5Y cells was decreased. The expression of microRNA-181a (miR-181a) was upregulated More >

  • Open Access

    ARTICLE

    MicroRNA-181a is elevated by 10-hydroxycamptothecin and represses lung carcinoma progression by downregulating FOXP1

    LI PAN1, WENTING YI2, DONGMIN LIANG1, YULONG ZHAO1, RANRAN WANG1, PINGYU WANG1, YOUJIE LI1, JIAXUAN XIN1, YUNFEI YAN1,*,#, SHUYANG XIE1,*,#

    BIOCELL, Vol.46, No.2, pp. 417-431, 2022, DOI:10.32604/biocell.2022.015522

    Abstract Tumor progression is usually characterized by proliferation, migration, and angiogenesis, which is essential for supplying both nutrients and oxygen to the tumor cells. Therefore, targeting angiogenesis has been considered a promising therapeutic strategy for cancer prevention and treatment. In the present study, we demonstrated that in addition to suppressing lung cancer cell proliferation and migration in vitro, 10-hydroxycamptothecin (10-HCPT) is also capable of inhibiting angiogenesis in vivo with a miR-181a-dependent manner. Mechanistically, by upregulating miR-181a, which in turn downregulating FOXP1, 10-HCPT can inhibit the PI3K/Akt/ERK signaling pathwaymediated angiogenesis. Furthermore, reduced levels of miR-181a have been found in More >

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