Knockdown of long non-coding RNA XIST exerts tumor-suppressive functions in human glioblastoma stem cells by up-regulating miR-152.

Glioblastoma (GBM) is the most common and aggressive primary brain tumor. Great interest persists in useful therapeutic targets in GBM. Aberrant expression of long non-coding RNAs (lncRNAs) has been functionally associated with many cancers. Here, we elucidated the function and the possible molecular mechanisms of lncRNA XIST in human glioblastoma stem cells (GSCs). Our results proved that XIST expression was up-regulated in glioma tissues and GSCs. Functionally, knockdown of XIST exerted tumor-suppressive functions by reducing cell proliferation, migration and invasion as well as inducing apoptosis. The in vivo studies also showed that knockdown of XIST suppressed tumor growth and produced high survival in nude mice. Further, there was reciprocal repression between XIST and miR-152. Mechanistic investigations defined the direct binding ability of the predicted miR-152 binding site on the XIST. In addition, XIST and miR-152 are probably in the same RNA induced silencing complex (RISC). Finally, miR-152 mediated the tumor-suppressive effects that knockdown of XIST exerted. Taken together, these results provided a comprehensive analysis of XIST in GSCs and important clues for understanding the key roles of lncRNA-miRNA functional network in human glioma.

Yao Y ，Ma J ，Xue Y ，Wang P ，Li Z ，Liu J ，Chen L ，Xi Z ，Teng H ，Wang Z ，Li Z ，Liu Y ... -  《-》

Knockdown of long non-coding RNA HOTAIR inhibits malignant biological behaviors of human glioma cells via modulation of miR-326.

Ke J ，Yao YL ，Zheng J ，Wang P ，Liu YH ，Ma J ，Li Z ，Liu XB ，Li ZQ ，Wang ZH ，Xue YX ... -  《Oncotarget》

MiR-152 functions as a tumor suppressor in glioblastoma stem cells by targeting Krüppel-like factor 4.

Glioblastoma (GBM) is the most common central nervous system tumor and the molecular mechanism driving its development is still largely unknown, limiting the treatment of this disease. In the present study, we explored the potential role of miR-152 in glioblastoma stem cells (GSCs) as well as the possible molecular mechanisms. Our results proved that miR-152 was down-regulated in human GSCs. Restoring the expression of miR-152 dramatically reduced the cell proliferation, cell migration and invasion as well as inducing apoptosis. Mechanistic investigations defined Krüppel-like factor 4 (KLF4) as a direct and functional downstream target of miR-152, which was involved in the miR-152-mediated tumor-suppressive effects in GSCs. Meanwhile, this process was coincided with the down-regulated LGALS3 that could be bound and promoted by KLF4, leading to attenuate the activation of MEK1/2 and PI3K signal pathways. Moreover, the in vivo study showed that miR-152 over-expression and KLF4 knockdown produced the smallest tumor volume and the longest survival in nude mice. Taken together, these results elucidated the function of miR-152 in GSCs progression and suggested a promising application of it in glioma treatment.

Ma J ，Yao Y ，Wang P ，Liu Y ，Zhao L ，Li Z ，Li Z ，Xue Y ... -  《-》

CRNDE affects the malignant biological characteristics of human glioma stem cells by negatively regulating miR-186.

Zheng J ，Li XD ，Wang P ，Liu XB ，Xue YX ，Hu Y ，Li Z ，Li ZQ ，Wang ZH ，Liu YH ... -  《Oncotarget》

Knockdown of SOX2OT inhibits the malignant biological behaviors of glioblastoma stem cells via up-regulating the expression of miR-194-5p and miR-122.

Su R ，Cao S ，Ma J ，Liu Y ，Liu X ，Zheng J ，Chen J ，Liu L ，Cai H ，Li Z ，Zhao L ，He Q ，Xue Y ... -  《Molecular Cancer》