Home / Advanced Search

  • Title/Keywords

  • Author/Affliations

  • Journal

  • Article Type

  • Start Year

  • End Year

Update SearchingClear
  • Articles
  • Online
Search Results (2)
  • Open Access

    ARTICLE

    NOTCH3 Overexpression and Posttranscriptional Regulation by miR-150 Were Associated With EGFR–TKI Resistance in Lung Adenocarcinoma

    Youwei Zhang*, Bi Chen, Yongsheng Wang, Qi Zhao, Weijun Wu§, Peiying Zhang*, Liyun Miao, Sanyuan Sun*

    Oncology Research, Vol.27, No.7, pp. 751-761, 2019, DOI:10.3727/096504018X15372657298381

    Abstract Acquired resistance remains a key challenge in epidermal growth factor receptor (EGFR)–tyrosine kinase inhibitors (TKIs) therapy in lung adenocarcinoma (LUAD). Recent studies have shown that Notch signaling is associated with drug resistance. However, its role and possible mechanisms in EGFR-TKI resistance are not yet clear. In our study, we found that among four members of NOTCH1–4, only NOTCH3 was upregulated in LUAD tissues and TKI-resistant cell line (HCC827GR6). Knockdown of NOTCH3 by siRNA significantly inhibited proliferative ability, and decreased colony and sphere formation in HCC827GR6 cells. Then miR-150 was identified as a posttranscriptional regulator of NOTCH3. Its expression was downregulated… More >

  • Open Access

    ARTICLE

    miR-150 Suppresses Tumor Growth in Melanoma Through Downregulation of MYB

    Xiyan Sun*1, Chao Zhang†1, Yang Cao, Erbiao Liu*

    Oncology Research, Vol.27, No.3, pp. 317-323, 2019, DOI:10.3727/096504018X15228863026239

    Abstract miR-150 has been demonstrated to inhibit tumor progression in various human cancers, including colorectal cancer, ovarian cancer, and thyroid cancer. However, the role of miR-150 in melanoma remains to be determined. In this study, we found that miR-150 was underexpressed in melanoma tissues and cell lines. Through transfection of miR-150 mimics, we found that miR-150 significantly inhibited the proliferation, migration, and invasion of melanoma cells. In mechanism, we found that MYB was a target of miR-150 in melanoma cells. Overexpression of miR-150 significantly inhibited mRNA and protein levels of MYB in melanoma cells. Moreover, there was an inverse correlation between… More >

Displaying 1-10 on page 1 of 2. Per Page