scholarly journals Long noncoding RNA LINC00968 inhibits proliferation, migration and invasion of lung adenocarcinoma through targeting miR-22-5p/CDC14A axis

3 Biotech ◽  
2021 ◽  
Vol 11 (10) ◽  
Author(s):  
Chao Wu ◽  
Xuzhao Bian ◽  
Liyuan Zhang ◽  
Yuanyuan Hu ◽  
Yang Wu ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Migration And Invasion

scholarly journals Knockdown of Long Noncoding RNA (lncRNA) Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1) Inhibits Proliferation, Migration, and Invasion and Promotes Apoptosis by Targeting miR-124 in Retinoblastoma

2018 ◽  
Vol 26 (4) ◽  
pp. 581-591 ◽  
Author(s):  
Shujun Liu ◽  
Guigang Yan ◽  
Junfu Zhang ◽  
Lianzhi Yu
Keyword(s):  
Lung Adenocarcinoma ◽  
Cell Viability ◽  
Cell Line ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Migration And Invasion ◽  
Erk Mapk ◽  
Underlying Mechanisms ◽  
Y79 Cells

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.

scholarly journals Long Noncoding RNA RGMB-AS1 Indicates a Poor Prognosis and Modulates Cell Proliferation, Migration and Invasion in Lung Adenocarcinoma

PLoS ONE ◽  
2016 ◽  
Vol 11 (3) ◽  
pp. e0150790 ◽  
Author(s):  
Ping Li ◽  
Guojun Zhang ◽  
Juan Li ◽  
Rui Yang ◽  
Shanshan Chen ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Lung Adenocarcinoma ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Poor Prognosis ◽  
Migration And Invasion

scholarly journals The long noncoding RNA LINC00483 promotes lung adenocarcinoma progression by sponging miR-204-3p

2019 ◽  
Vol 24 (1) ◽  
Author(s):  
Shengzhuang Yang ◽  
Tao Liu ◽  
Yu Sun ◽  
Xiangsen Liang
Keyword(s):  
Cell Proliferation ◽  
Lung Adenocarcinoma ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Clinicopathological Characteristics ◽  
Positive Lymph Node ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Survival Times ◽  
The Impact

Abstract Background The expression of the long noncoding RNA LINC00483 is upregulated in lung adenocarcinoma (LUAD). However, its role in the progression of LUAD and the underlying mechanisms remain elusive. Methods The expressions of LINC00483 and miR-204-3p were determined using quantitative real-time PCR. The correlation between the clinicopathological characteristics of LUAD patients and LINC00483 expression was analyzed using Pearson’s χ2 test. A549 and PC-9 cells were transfected with small interfering RNA (siRNA) that specially targeting LINC00483 to assess the impact of its knockdown. Cell proliferation was assessed using the Cell Counting Kit-8 and clone forming assays. Cell migration and cell invasion were evaluated using a transwell assay. The levels of Snail, E-cadherin, N-cadherin and ETS1 proteins were determined via western blotting. The interaction between LINC00483 and miR-204-3p was analyzed using dual-luciferase, fluorescence in situ hybridization and RNA immunoprecipitation. Results LINC00483 was upregulated in LUAD tissues and cell lines. Higher LINC00483 levels closely correlated to shorter survival times, advanced TNM stage, larger tumor size and positive lymph node metastasis. Cell proliferation, migration and invasion were suppressed after LINC00483 knockdown. LINC00483 mainly localized in the cytoplasm, where it acted as a sponge of miR-204-3p. ETS1 was validated as a downstream target of miR-204-3p and is thus regulated by LINC00483. Conclusion This study demonstrated that LINC00483 facilitates the proliferation, migration and invasion of LUAD cells by acting as a sponge for miR-204-3p, which in turn regulates ETS1.

Long noncoding RNA LINC00520 accelerates lung adenocarcinoma progression via miR-1252-5p/FOXR2 pathway

Human Cell ◽  
2021 ◽  
Vol 34 (2) ◽  
pp. 478-490
Author(s):  
Xinyue Chen ◽  
Huimin Chen ◽  
Miaowen Liu ◽  
Jianping Xiong ◽  
Zhiwang Song
Keyword(s):  
Lung Adenocarcinoma ◽  
Long Noncoding Rna ◽  
Noncoding Rna

scholarly journals PRKAR1B-AS2 Long Noncoding RNA Promotes Tumorigenesis, Survival, and Chemoresistance via the PI3K/AKT/mTOR Pathway

2021 ◽  
Vol 22 (4) ◽  
pp. 1882
Author(s):  
Abdelrahman M. Elsayed ◽  
Emine Bayraktar ◽  
Paola Amero ◽  
Salama A. Salama ◽  
Abdelaziz H. Abdelaziz ◽  
...  
Keyword(s):  
Mouse Model ◽  
Long Noncoding Rna ◽  
Proteomic Analysis ◽  
Noncoding Rna ◽  
Mtor Pathway ◽  
The Cancer Genome Atlas ◽  
Migration And Invasion ◽  
Physical Interaction ◽  
Cisplatin Sensitivity

Many long noncoding RNAs have been implicated in tumorigenesis and chemoresistance; however, the underlying mechanisms are not well understood. We investigated the role of PRKAR1B-AS2 long noncoding RNA in ovarian cancer (OC) and chemoresistance and identified potential downstream molecular circuitry underlying its action. Analysis of The Cancer Genome Atlas OC dataset, in vitro experiments, proteomic analysis, and a xenograft OC mouse model were implemented. Our findings indicated that overexpression of PRKAR1B-AS2 is negatively correlated with overall survival in OC patients. Furthermore, PRKAR1B-AS2 knockdown-attenuated proliferation, migration, and invasion of OC cells and ameliorated cisplatin and alpelisib resistance in vitro. In proteomic analysis, silencing PRKAR1B-AS2 markedly inhibited protein expression of PI3K-110α and abrogated the phosphorylation of PDK1, AKT, and mTOR, with no significant effect on PTEN. The RNA immunoprecipitation detected a physical interaction between PRKAR1B-AS2 and PI3K-110α. Moreover, PRKAR1B-AS2 knockdown by systemic administration of 1,2-dioleoyl-sn-glycero-3-phosphatidylcholine nanoparticles loaded with PRKAR1B-AS2–specific small interfering RNA enhanced cisplatin sensitivity in a xenograft OC mouse model. In conclusion, PRKAR1B-AS2 promotes tumor growth and confers chemoresistance by modulating the PI3K/AKT/mTOR pathway. Thus, targeting PRKAR1B-AS2 may represent a novel therapeutic approach for the treatment of OC patients.

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