Abstract
Through epithelial-mesenchymal transition (EMT), cancer cells acquire enhanced ability of migration and invasion, stem cell like characteristics and therapeutic resistance. Notch signaling regulates cell-cell connection, cell polarity and motility during organ development. Recent studies demonstrate that Notch signaling plays an important role in lung cancer initiation and cross-talks with several transcriptional factors to enhance EMT, contributing to the progression of non-small cell lung cancer (NSCLC). Correspondingly, blocking of Notch signaling inhibits NSCLC migration and tumor growth by reversing EMT. Clinical trials have showed promising effect in some cancer patients received treatment with Notch1 inhibitor. This review attempts to provide an overview of the Notch signal in NSCLC: its biological significance and therapeutic application.Electronic supplementary materialThe online version of this article (doi:10.1186/s13045-014-0087-z) contains supplementary material, which is available to authorized users.
Highlights
Through epithelial-mesenchymal transition (EMT), cancer cells acquire enhanced ability of migration and invasion, stem cell like characteristics and therapeutic resistance
NCI SEER database reported that 5-year survival was 58.2% for non-small cell lung cancer (NSCLC) patients diagnosed at localized stage (18%) of all stages including localized, regional and distant from 2004–2010, whereas it was only 4.5% when diagnosed at distant stage (55%) [3]
EMT, metastases and drug resistance are intertwined in NSCLC, which lead to aggravation and poor prognosis
Summary
Through epithelial-mesenchymal transition (EMT), cancer cells acquire enhanced ability of migration and invasion, stem cell like characteristics and therapeutic resistance. By inhibiting epithelial-mesenchymal transition (EMT), silencing MALAT1 reduced lung cancer cell invasion and metastasis. Either dominant-negative Notch3 receptor [58] or MRK-003, a gamma-secretase inhibitor [59], antagonized Notch3 signaling, attenuated cell growth, and induced apoptosis of lung cancer cell lines.
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