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 >
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