Gliomas are characterized by high incidence, recurrence and mortality all of which are significant challenges to efficacious clinical treatment. The hypoxic microenvironment in the inner core and intermediate layer of the
tumor mass of
gliomas is a critical contributor to
glioma pathogenesis. In this study, we identified an upregulated
lncRNA, OR7E156P, in
glioma was identified. The silencing of OR7E156P inhibited cell invasion and
DNA synthesis in vitro and
tumor growth in vivo. OR7E156P was intricately linked to the HIF1A pathway.
Hypoxia could induce OR7E156P expression, whereas OR7E156P silencing decreased HIF1A
protein levels under hypoxic conditions.
Hypoxia promoted
glioma cell invasion and
DNA synthesis, and HUVEC tube formation, whereas OR7E156P silencing partially reversed the cellular effects of
hypoxia. HIF1A overexpression promoted, whereas OR7E156P silencing inhibited
tumor growth; the inhibitory effects of OR7E156P silencing on
tumor growth were partially reversed by HIF1A overexpression. miR-143 directly targeted OR7E156P and HIF1A, respectively. miR-143 inhibition increased HIF1A
protein levels, promoted
glioma cell invasion and
DNA synthesis. Moreover, they enhanced HUVEC tube formation, whereas OR7E156P silencing partially reversed the cellular effects of miR-143 inhibition. HIF1A targeted the promoter region of miR-143 and inhibited miR-143 expression. Altogether a regulatory axis consisting of OR7E156P, miR-143, and HIF1A, was identified which is deregulated in
glioma, and the process of the OR7E156P/miR-143/HIF1A axis modulating
glioma cell invasion through ZEB1 and HUVEC tube formation through
VEGF was demonstrated.