These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: microRNA-381 suppresses the growth and increases cisplatin sensitivity in non-small cell lung cancer cells through inhibition of nuclear factor-κB signaling.
    Author: Huang RS, Zheng YL, Zhao J, Chun X.
    Journal: Biomed Pharmacother; 2018 Feb; 98():538-544. PubMed ID: 29287202.
    Abstract:
    microRNA (miR)-381 is downregulated and exhibits anti-invasive activity in non-small cell lung cancer (NSCLC). In this study, we investigated the role of miR-381 in proliferation, tumorigenesis, and cisplatin resistance of NSCLC cells. The effects of miR-381 overexpression on proliferation, tumorigenesis, cell cycle progression, and cisplatin sensitivity were examined. Overexpression of miR-381 significantly inhibited cell proliferation and colony formation in vitro and tumorigenesis in vivo. Ectopic expression of miR-381 arrested NSCLC cells at G0/G1 phase, which was accompanied by increased expression of p21 and p27 and decreased expression of cyclin D1 and CDK4. Compared to A549 parental cells, cisplatin-resistant equivalents (A549/CDDP) had reduced levels of miR-381. miR-381 re-sensitized A549/CDDP cells to cisplatin and potentiated cisplatin-induced apoptosis. Mechanistically, miR-381 interfered with the activation of nuclear factor (NF)-κB through repression of inhibitor of differentiation 1 (ID1). Co-expression of ID1 reversed the suppression of proliferation and enhancement of cisplatin cytotoxicity by miR-381. Taken together, miR-381 can induce growth suppression and chemosensitization in NSCLC, largely through inactivation of NF-κB via downregulation of ID1. Restoration of miR-381 represents a potential therapeutic strategy for NSCLC.
    [Abstract] [Full Text] [Related] [New Search]