The human
metastasis associated
lung adenocarcinoma transcript 1 (MALAT1) is a
long non-coding RNA associated with
metastasis, and is a favorable prognostic factor for
lung cancer. Recent studies have shown that MALAT1 plays an important role in many
malignancies. However, little is known about the role of MALAT1 in
glioma. In this study, we determined the expression of MALAT1 and explored its prognostic value in
glioma. Further, we investigated the regulatory mechanism of MALAT1 in
glioma progression. Our results showed that the expression of MALAT1 was significantly decreased in
glioma specimens than in noncancerous brain tissues. In addition, MALAT1 expression was significantly correlated with
tumor size, WHO grade and Karnofsky Performance Status (KPS), and was an independent prognostic factor for survival of
glioma patients. The gain- and loss-of-function experiments revealed miR-155 down-regulation by MALAT1, resulting in reciprocal effects. Further, MALAT1 suppresses cell viability by down-regulating miR-155. FBXW7
mRNA was identified as a direct target of miR-155 in
glioma. The miR-155-induced
tumorigenesis is mediated through FBXW7 function. Finally, we found that MALAT1 positively regulated FBXW7 expression, which was responsible for
glioma progression mediated by MALAT1-miR-155 pathway. In conclusion, our data demonstrated that MALAT1 may be a novel prognostic
biomarker and therapeutic target in
glioma. Restoration of MALAT1 levels represents a novel therapeutic strategy against
glioma.