scholarly journals Long Noncoding RNA HOXB-AS1 Is Upregulated in Endometrial Carcinoma and Sponged miR-149-3p to Upregulate Wnt10b

2020 ◽  
Vol 19 ◽  
pp. 153303382096746
Author(s):  
Da Liu ◽  
Min Qiu ◽  
Lili Jiang ◽  
Kuiran Liu

The functions of Long noncoding RNA (lncRNA) HOXB-AS1 have been investigated in glioblastoma and multiple myeloma. However, the role of lncRNA HOXB-AS1 in endometrial carcinoma (EC) remains largely unknown. This study investigated the underlying mechanisms of the lncRNA HOXB-AS1 on the progression of EC. In this study, We found that HOXB-AS1 expression was significantly upregulated in EC tissue samples and was associated with shorter survival time. Furthermore, upregulation of HOXB-AS1 promoted proliferation, invasion, and migration of EC cell. HOXB-AS1 and Wnt10b directly bound to miR-149-3p. HOXB-AS1 increased the expression of Wnt10b by binding to miR-149-3p. We further verified the upregulation of β-catenin, cyclin D1, and c-myc induced by HOXB-AS1. In conclusion, our results indicated that HOXB-AS1 exerted oncogenic function as competing endogenous RNA (ceRNA) of miR-149-3p to release Wnt10b and activated Wnt/β-catenin pathway.

2018 ◽  
Vol Volume 11 ◽  
pp. 7483-7492 ◽  
Author(s):  
Jing Wu ◽  
Mingyu Du ◽  
Qian Zhang ◽  
Wenjun Zhang ◽  
Yanxin Fan ◽  
...  

Author(s):  
Shujun Liu ◽  
Guigang Yan ◽  
Junfu Zhang ◽  
Lianzhi Yu

Evidence suggests that the long noncoding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is upregulated in cancer tissues, and its elevated expression is associated with hyperproliferation. However, the underlying mechanisms regarding the role of MALAT1 in retinoblastoma (RB) remain unclear. This study aimed to explore the functional role of MALAT1 in RB by targeting miR-124. The results showed that the expression of MALAT1 was significantly higher in the Y79 cell line than in the ARPE-19 cell line (p < 0.01). Moreover, MALAT1 silence inhibited cell viability, migration, and invasion and promoted apoptosis in Y79 cells (p < 0.05, p < 0.01, or p < 0.001). miR-124 was upregulated by MALAT1 silence and hence was identified as a target of MALAT1 (p < 0.05 or p < 0.001). In addition, miR-124 suppression inhibited cell apoptosis and remarkably abolished the inhibitory effects of MALAT1 silence on cell viability, migration, and invasion (p < 0.05, p < 0.01, or p < 0.001). In addition, Slug was a target of miR-124 and regulated cell viability, migration, invasion, and apoptosis in Y79 cells (p < 0.05, p < 0.01, or p < 0.001). Further, Slug silence abolished miR-124 suppression-induced inactivation of the ERK/MAPK and Wnt/β-catenin pathways. Taken together, our data highlight the pivotal role of MALAT1 in RB. Moreover, the present study elucidated the MALAT1‐miR-124‐ERK/MAPK and Wnt/β-catenin signaling pathways in RB, which might provide a new approach for the treatment of RB.


2019 ◽  
Vol 39 (1) ◽  
Author(s):  
Wei-Li Sun ◽  
Tian Kang ◽  
Yuan-Yu Wang ◽  
Jian-Ping Sun ◽  
Chen Li ◽  
...  

Abstract The present study was undertaken to investigate the underlying mechanisms of long noncoding RNA OIP5-AS1 via regulating miR-410 to modulate Wnt-7b in the progression of glioma. To address this problem, we measured the expression of OIP5-AS1 and miR-410 in glioma tissues by qRT-PCR. Glioma U87 cells were transfected with OIP5-AS1 siRNA or miR-410 inhibitors. The targeting relationships among miR-410, OIP5-AS1 and Wnt-7b were verified by luciferase reporter assays. Western blotting was employed to determine the expression of Wnt-7b/β-catenin pathway-related proteins, while MTT, flow cytometry, Transwell assays and wound-healing assays were used to measure the biological characteristics of glioma cells. The results showed that OIP5-AS1 expression was higher and miR-410 was lower in glioma tissues. Luciferase reporter assays confirmed a targeting relationship between OIP5-AS1 and miR-410, as well as between miR-410 and Wnt-7b. Silencing OIP5-AS1 reduced cell proliferation, invasion and migration of glioma U87 cells and led to depressed expression levels of miR-410, Wnt-7b, p-β-catenin, GSK-3β-pS9, c-Myc and cyclin D1. Furthermore, down-regulation of OIP5-AS1 induced G0/G1 phase cell cycle arrest and apoptosis of glioma cells. Inhibitors of miR-410 abolished the biological effects of OIP5-AS1 siRNA in glioma cells. In vivo, OIP5-AS1 knockdown also inhibited tumor growth. Taken together, this research suggested that silencing OIP5-AS1 may specifically block the Wnt-7b/β-catenin pathway via targeted up-regulating miR-410, thereby inhibiting growth, invasion and migration while promoting apoptosis in glioma cells.


2017 ◽  
Vol 119 (2) ◽  
pp. 1827-1840 ◽  
Author(s):  
Xin Wen ◽  
Xin‐Rui Han ◽  
Yong‐Jian Wang ◽  
Shao‐Hua Fan ◽  
Juan Zhuang ◽  
...  

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