scholarly journals MiR-1224-5p Activates Autophagy, Cell Invasion and Inhibits Epithelial-to-Mesenchymal Transition in Osteosarcoma Cells by Directly Targeting PLK1 Through PI3K/AKT/mTOR Signaling Pathway

2020 ◽  
Vol Volume 13 ◽  
pp. 11807-11818
Author(s):  
Bicheng Jin ◽  
Dongfang Jin ◽  
Zhaozhen Zhuo ◽  
Bo Zhang ◽  
Kun Chen
Keyword(s):  
Signaling Pathway ◽  
Cell Invasion ◽  
Epithelial To Mesenchymal Transition ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Osteosarcoma Cells ◽  
Mesenchymal Transition

DNMT1-mediated lncRNA MEG3 methylation accelerates endothelial-mesenchymal transition in diabetic retinopathy through the PI3K/AKT/mTOR signaling pathway

2020 ◽  
Author(s):  
Yue He ◽  
Yujiao Dan ◽  
Xiaorong Gao ◽  
Li Huang ◽  
Hongbin Lv ◽  
...  
Keyword(s):  
Diabetic Retinopathy ◽  
Signaling Pathway ◽  
Dna Methyltransferase ◽  
Cell Model ◽  
Mtor Signaling ◽  
Diabetic Patients ◽  
Cell Models ◽  
Mtor Signaling Pathway ◽  
Mesenchymal Transition ◽  
Endothelial Mesenchymal Transition

Diabetic retinopathy (DR) is one of the serious complications that occur in diabetic patients that frequently causes blindness. Long non-coding RNAs (lncRNAs) have been associated with DR pathology. This study aimed to determine the underlying mechanism of lncRNA maternally expressed gene 3 (MEG3) in association with DNA methyltransferase 1 (DNMT1) in the endothelial-mesenchymal transition (endMT) that occurs in DR. A rat model of DR was induced by streptozotocin (STZ) injection, and high glucose (HG)-induced cell model was established by exposing microvascular endothelial cells obtained from retina of rats to HG. Subsequently, MEG3 was overexpressed in rat and cell models to characterize its impact on endMT in DR and the involvement of the PI3K/AKT/mTOR signaling pathway. Furthermore, the methylation level of MEG3 promoter region was determined with the application of methylation-specific polymerase chain reaction, followed by Chromatin immunoprecipitation assay for methyltransferase enrichment. Finally, we examined the regulation of DNMT1 on MEG3 methylation and endMT in the HG-induced cell model. The results obtained revealed downregulated MEG3 expression in DR rat and cell models. Overexpressed MEG3 was shown to suppress endMT in DR rat and cell models through the inhibition of the PI3K/AKT/mTOR signaling pathway. Notably, DNMT1 could promote MEG3 promoter methylation to inhibit MEG3 expression by recruiting methyltransferase, which activated the PI3K/AKT/mTOR signaling pathway to accelerate endMT in DR. These findings further highlighted the inhibitory effect of MEG3 on endMT in DR, thus presenting a novel therapeutic target candidate for DR treatment.

MiR-92a-3p promotes the malignant progression of hepatocellular carcinoma by mediating the PI3K/AKT/mTOR signaling pathway

2021 ◽  
Vol 27 ◽  
Author(s):  
Libing Wang ◽  
Mingxin Cui ◽  
Fengzhi Qu ◽  
Daming Cheng ◽  
Jingkun Yu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Western Blot ◽  
Signaling Pathway ◽  
Epithelial Mesenchymal Transition ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Mesenchymal Transition ◽  
Diagnosis And Prognosis ◽  
Potential Biomarker ◽  
Hcc Cells

Background: As one of the most common cancers in the world, hepatocellular carcinoma (HCC) usually has a poor prognosis. Many HCC patients are usually diagnosed at advanced stages. Therefore, new potential biomarkers for the diagnosis and prognosis of HCC are urgently needed. More and more studies have shown that miR-92a-3p can regulate the occurrence and development of a variety of cancers, but its clinical significance and molecular mechanism in HCC are still elusive. Here, we tried to clarify the regulatory mechanism of miR-92a-3p in HCC. Methods: In this study, we conducted qRT-PCR and revealed that miR-92a-3p was notably upregulated in HCC cells. MTT, flow cytometry, wound healing, Transwell invasion assays and western blot were conducted to uncover that overexpressed miR-92a-3p could boost the proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) of HCC cells while inhibiting cell apoptosis. In addition, the proteins associated with PI3K/AKT/mTOR pathway were also detected by western blot. Results: It was suggested that miR-92a-3p could activate the PI3K/AKT/mTOR signaling pathway. Conclusion: These results suggest that miR-92a-3p plays a tumor-promoting role in HCC and may be a potential biomarker for the diagnosis and prognosis of HCC.

scholarly journals YTHDF1 promotes hepatocellular carcinoma progression via activating PI3K/AKT/mTOR signaling pathway and inducing epithelial-mesenchymal transition

2021 ◽  
Vol 10 (1) ◽  
Author(s):  
Xiangyuan Luo ◽  
Mengdie Cao ◽  
Fan Gao ◽  
Xingxing He
Keyword(s):  
Signaling Pathway ◽  
Rna Binding ◽  
Epithelial Mesenchymal Transition ◽  
Mtor Signaling ◽  
Gene Set Enrichment Analysis ◽  
Migration And Invasion ◽  
Mtor Signaling Pathway ◽  
Promoting Effect ◽  
Mesenchymal Transition ◽  
Hcc Cells

Abstract Background N6-methyladenosine (m6A) modification, as the most abundant RNA modification, widely participates in the physiological process and is involved in multiple disease progression, especially cancer. YTH N6-methyladenosine RNA binding protein 1 (YTHDF1) is a pivotal m6A “reader” protein, which has been reported in multiple cancers. However, the role and molecular mechanism of YTHDF1 in HCC are still not fully elucidated. Methods Based on various bioinformatics databases, q-RT PCR, western blot, and a tissue microarray containing 90 HCC samples, we examined the expression of YTHDF1 in HCC. Then, we applied the loss-of-function experiments to explore the role of YTHDF1 in HCC by in vitro and in vivo assays. Finally, we performed the gene set enrichment analysis (GSEA) to predict the potential signaling pathway of YTHDF1 involved in HCC and further verified this prediction. Results YTHDF1 was overexpressed in HCC and associated with HCC grade. Depletion of YTHDF1 markedly impaired the proliferation, migration, invasion, and cell cycle process of HCC cells. Mechanistically, YTHDF1 promoted the growth of HCC cells via activating the PI3K/AKT/mTOR signaling pathway. Moreover, we also demonstrated that the epithelial-mesenchymal transition (EMT) mediated the promoting effect of YTHDF1 on the migration and invasion of HCC cells. Conclusions YTHDF1 contributes to the progression of HCC by activating PI3K/AKT/mTOR signaling pathway and inducing EMT.

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