Long‐noncoding RNA HOTAIR inhibits immunologic rejection of mouse leukemia cells through activating the Wnt/β‐catenin signaling pathway in a mouse model of leukemia

2019 ◽  
Vol 234 (7) ◽  
pp. 10386-10396 ◽  
Author(s):  
Guo‐Jie Li ◽  
Hui Ding ◽  
Dong Miao
Keyword(s):  
Mouse Model ◽  
Signaling Pathway ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Leukemia Cells ◽  
Mouse Leukemia

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.

Long Noncoding RNA HOXA Cluster Anti-Sense RNA 2 Inhibits Mycoplasma pneumoniae-Induced Inflammation by Regulating the Nuclear Factor-KappaB Signaling Pathway

2021 ◽  
Vol 11 (11) ◽  
pp. 2262-2273
Author(s):  
Mei Feng ◽  
Chengjie Zhuo ◽  
Xuefen Zhu
Keyword(s):  
Cell Viability ◽  
Signaling Pathway ◽  
Mycoplasma Pneumoniae ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Flow Cytometric Analysis ◽  
Inflammatory Factors ◽  
Epithelial Cell Line ◽  
Inflammatory Factor ◽  
Hoxa Cluster

Mycoplasma pneumoniae (MP) is the primary cause of community-acquired lung inflammation. The MP-induced manifestations of pneumonia are associated with the release of pro-inflammatory cytokines; however, the mechanisms of MP-induced inflammation have not been fully clarified. The purpose of the present study was to determine whether long noncoding RNA HOXA cluster anti-sense RNA 2 (lncRNA HOXA-AS2) is involved in MP-induced inflammation. A model of MP-induced cellular inflammation was established using the human BEAS-2B lung epithelial cell line and lncRNA HOXA-AS2 levels were detected using reverse transcription-quantitative (RT-q) PCR. MTT and flow cytometric analysis were used to assess cell viability and apoptosis, respectively. The secretion of pro-inflammatory factors including tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6 were measured by ELISA, and protein levels of phosho- (p-)p65 and p-NF-κB inhibitor α (p-IκBα) were detected by western blotting. The results suggest that MP infection significantly decreases the level of lncRNA HOXA-AS2 in BEAS-2B cells. lncRNA HOXA-AS2 overexpression significantly enhanced cell viability, inhibited apoptosis, decreased pro-inflammatory factor expression (TNF-α, IL-β and IL-6) and inhibited NF-κB pathway activation in MP-stimulated BEAS-2B cells. Conversely, lncRNA HOXA-AS2-knockdown resulted in the opposite effects. In conclusion, lncRNA HOXA-AS2 is involved in MP infection-induced inflammation and regulates the NF-κB signaling pathway.

A novel long noncoding RNA FAF inhibits apoptosis via upregulating FGF9 through PI3K/AKT signaling pathway in ischemia–hypoxia cardiomyocytes

2019 ◽  
Vol 234 (12) ◽  
pp. 21973-21987 ◽  
Author(s):  
Hao‐Jie Shi ◽  
Ming‐Wei Wang ◽  
Jia‐Teng Sun ◽  
Hao Wang ◽  
Ya‐Fei Li ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Akt Signaling ◽  
Akt Signaling Pathway

scholarly journals Long noncoding RNA MALAT1 contributes to inflammatory response of microglia following spinal cord injury via the modulation of a miR-199b/IKKβ/NF-κB signaling pathway

2018 ◽  
Vol 315 (1) ◽  
pp. C52-C61 ◽  
Author(s):  
Heng-Jun Zhou ◽  
Li-Qing Wang ◽  
Duan-Bu Wang ◽  
Jian-Bo Yu ◽  
Yu Zhu ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Inflammatory Response ◽  
Signaling Pathway ◽  
Proinflammatory Cytokines ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Tnf Α ◽  
Cord Injury

Long noncoding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) was widely recognized to be implicated in human cancer, vascular diseases, and neurological disorders. This study was to explore the role and underlying mechanism of MALAT1 in acute spinal cord injury (ASCI). ASCI models in adult rats were established and demonstrated by a numerical decrease in BBB scores. Expression profile of MALAT1 and miR-199b following ASCI in rats and in vitro was determined using quantitative real-time PCR. RNA pull-down assays combined with RIP assays were performed to explore the interaction between MALAT1 and miR-199b. In the present study, MALAT1 expression was significantly increased (2.4-fold that of control) in the spinal cord of the rat contusion epicenter accompanied by activation of IKKβ/NF-κB signaling pathway and an increase in the level of proinflammatory cytokines TNF-α and IL-1β. Upon treatment with LPS, MALAT1 expression dramatically increased in the microglia in vitro, but knockdown of MALAT1 attenuated LPS-induced activation of MGs and TNF-α and IL-1β production. Next, we confirmed that LPS-induced MALAT1 activated IKKβ/NF-κB signaling pathway and promoted the production of proinflammatory cytokines TNF-α and IL-1β through downregulating miR-199b. More importantly, MALAT1 knockdown gradually improved the hindlimb locomotor activity of ASCI rats as well as inhibited TNF-α, IL-1β levels, and Iba-1 protein, the marker of activated microglia in injured spinal cords. Our study demonstrated that MALAT1 was dysregulated in ASCI rats and in LPS-activated MGs, and MALAT1 knockdown was expected to attenuate ASCI through repressing inflammatory response of MGs.

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