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LncRNA H19 downregulation confers erlotinib resistance through upregulation of PKM2 and phosphorylation of AKT in EGFR-mutant lung cancers.

Abstract：

:First-generation EGFR tyrosine kinase inhibitors (TKIs) such as erlotinib have significant activity in NSCLC patients with activating EGFR mutations. However, EGFR-TKI resistance inevitably occurs after approximately 12 months of treatment. Acquired mechanisms of resistance, other than secondary mutations in EGFR (T790 M) which account for 50-60%, are less well understood. Here, we identified lncRNA H19 as a significantly downregulated lncRNA in vitro models and clinical specimens with acquired EGFR-TKI resistance, H19 knockdown or overexpression conferred resistance or sensitivity, respectively, both in vitro and in vivo models. H19 downregulation contributed to erlotinib resistance through interaction and upregulation of PKM2, which enhanced the phosphorylation of AKT. AKT inhibitors restored the sensitivity of erlotinib-resistant cells to erlotinib. In EGFR-mutant patients treated with EGFR-TKIs, low H19 levels were associated with a shorter progression-free survival (PFS) (P = 0.021). These findings revealed a novel mechanism of low-level H19 in the regulation of erlotinib resistance in EGFR-mutant lung cancers. Combination of AKT inhibitors and EGFR-TKIs could be a rational therapeutic approach for some subgroups of EGFR-mutant lung cancer patients.

journal_name

Cancer Lett

journal_title

Cancer letters

authors

Chen C,Liu WR,Zhang B,Zhang LM,Li CG,Liu C,Zhang H,Huo YS,Ma YC,Tian PF,Qi Q,Li JJ,Tang Z,Zhang ZF,Giaccone G,Yue DS,Wang CL

doi

10.1016/j.canlet.2020.05.009

subject

Has Abstract

pub_date

2020-08-28 00:00:00

pages

58-70

eissn

0304-3835

issn

1872-7980

pii

S0304-3835(20)30244-5

journal_volume

486

pub_type

杂志文章

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