Knockdown of lncRNA HOXD-AS1 suppresses proliferation, migration and invasion and enhances cisplatin sensitivity of glioma cells by sponging miR-204.

Increasing evidence suggests the involvement of long noncoding RNAs (lncRNAs) in various biological process including cancer progression and drug resistance. LncRNA HOXD cluster antisense RNA 1 (HOXD-AS1) had been demonstrated to act as an oncogenic gene, contributing to the development and progression of several cancers. However, its functional role and molecular mechanism underlying glioma progression and cisplatin (DDP) resistance has not been well elucidated. In this study, we found that HOXD-AS1 was up-regulated in glioma tissues and cells and negatively correlated with survival time. HOXD-AS1 knockdown suppressed proliferation, migration and invasion as well as enhanced DDP sensitivity of glioma cells. Moreover, HOXD-AS1 could function as a miR-204 sponge in glioma cells. Overexpression of miR-204 could mimic the functional role of down-regulated HOXD-AS1 in glioma cells. Furthermore, miR-204 inhibition reversed the effect of HOXD-AS1 knockdown on cancer progression and DDP sensitivity of glioma cells. In conclusion, knockdown of HOXD-AS1 suppressed proliferation, migration and invasion and enhanced DDP sensitivity of glioma cells through sequestering miR-204, providing a promising therapeutic target for glioma patients.

Zhou H ，Ma Y ，Zhong D ，Yang L ... -  《-》

HOXD-AS1 confers cisplatin resistance in gastric cancer through epigenetically silencing PDCD4 via recruiting EZH2.

Ye Y ，Yang S ，Han Y ，Sun J ，Xv L ，Wu L ，Ming L ... -  《Open Biology》

The lncRNA EGFR-AS1 is linked to migration, invasion and apoptosis in glioma cells by targeting miR-133b/RACK1.

Glioblastoma multiforme (GBM) is the most common in situ neoplasms in central nervous system (CNS). However, the pathogenesis of GBM is poorly understood. Long noncoding RNAs (lncRNAs) have been implicated in GBM progression. In this study, we attempted to identify the biological role of the EGFR-AS1 in glioma cells and tissues, as well as reveal the molecular mechanism associated. The results indicated that lnc-EGFR-AS1 expression was increased in glioma cells and tissues. EGFR-AS1 knockdown suppressed proliferation, migration and invasion of glioma cells, but induced apoptosis. Additionally, lnc-EGFR-AS1 functioned as a sponge for miR-133b. Promoting lnc-EGFR-AS1 expression significantly reduced miR-133b expression. Furthermore, miR-133b could target the 3'-untranslated region (3'-UTR) of RACK1 and reduced its expression levels. What's more, lnc-EGFR-AS1 knockdown reduced RACK1 expression partly through enhancing miR-133b expression. In vivo experiments confirmed the anti-tumorigenesis capability of EGFR-AS1 knockdown. These findings elucidated that EGFR-AS1 accelerated cell proliferation, migration, invasion and prevented apoptosis in glioma cells by regulating miR-133b/RACK1, providing new insights for the diagnosis and molecular therapy of GBM.

Dong ZQ ，Guo ZY ，Xie J 《-》

Long Noncoding RNA HOXD-AS1 Promotes the Proliferation, Migration, and Invasion of Colorectal Cancer via the miR-526b-3p/CCND1 Axis.

Colorectal cancer (CRC) is one of the most common malignancies in the world. It has been reported that the abnormal expression of long noncoding RNA HOXD-AS1 promotes the development of CRC, while the mechanism is still unclear. The aim of this study is to investigate the effects of HOXD-AS1 on proliferation, migration, and invasion in CRC and explore the underlying mechanism. Quantitative real-time polymerase chain reaction was used to detect the expression levels of HOXD-AS1, miR-526b-3p, and cyclin D1 (CCND1) in CRC tissues and cells. Dual-luciferase reporter assay was applied to examine the interaction between miR-526b-3p and HOXD-AS1 or CCND1. In addition, cell proliferation ability was assessed by Cell Counting Kit-8 assay. Cell migration and invasion abilities were determined using transwell assay. Furthermore, Western blot assay was conducted to measure the protein expression of CCND1. HOXD-AS1 was highly expressed in CRC, and high expression of HOXD-AS1 was related to the poor prognosis of patients with CRC. MiR-526b-3p could be targeted by HOXD-AS1. Function experiment results revealed that miR-526b-3p inhibitor could reverse the suppressive effect of HOXD-AS1 knockdown on the proliferation, migration, and invasion of CRC cells. Moreover, CCND1 was a target of miR-526b-3p, and its overexpression could reverse the inhibitory effect of miR-526b-3p overexpression on the proliferation, migration, and invasion of CRC cells. In addition, CCND1 overexpression reversed the suppressive effect of HOXD-AS1 knockdown on the proliferation, migration, and invasion of CRC. HOXD-AS1 upregulated the expression of CCND1 to promote the proliferation, migration, and invasion of CRC through targeting miR-526b-3p. This provided a new theoretical basis for clinical anticancer research of CRC.

Yan F ，Ma Y ，Liu L ，Li L ，Deng J ，Sun J ... -  《-》

Long noncoding RNA DLGAP1-AS1 promotes the progression of glioma by regulating the miR-1297/EZH2 axis.

Liu L ，Li X ，Shi Y ，Chen H ... -  《Aging-US》