Glioblastoma (GBM) remains the most common and malignant
tumor of the human central nervous system. Increasing evidence has highlighted that
tumor cells with high
transferrin receptor (TFRC) expression show advantages in growth. Long noncoding RNAs (lncRNAs) are related to
glioma progression by mediating
microRNAs (
miRNAs). However, the underlying mechanism among TFRC,
miRNA and
lncRNA in GBM is limited. In the current study, we identified a new
lncRNA-induced signaling mechanism that regulates the TFRC levels in GBM. The TFRC level was higher in
glioma cell lines, and elevated TFRC expression promoted the proliferation and survival of
glioma cells. Further study showed that hsa-miR-144a-3p bound to the 3'-UTR of TFRC
mRNA and inhibited its expression, preventing the malignant properties of
glioma cells, such as proliferation and survival. We also found that the
lncRNA RP1-86C11.7 sponges hsa-miR-144-3p to suppress its protective role in
glioma. RP1-86C11.7 overexpression in
glioma cells elevated TFRC expression, increased the intracellular free
iron level, and deteriorated oncogenicity, with a significant reduction in hsa-miR-144-3p. By contrast, silencing RP1-86C11.7 upregulated the hsa-miR-144-3p level, resulting in decreased TFRC expression and repressed
glioma progression. However, the effect of silencing RP1-86C11.7 was reversed with simultaneous hsa-miR-144-3p inhibitor treatment: the TFRC level, intracellular
iron level and proliferation in
glioma cells increased. Mechanistically, our data indicated that RP1-86C11.7 exacerbates the malignant behavior of
glioma through the hsa-miR-144-3p/TFRC axis. RP1-86C11.7 may be a potential
biomarker or target to treat
glioma in the future.