Microrna‐139‐5p inhibits epithelial‐mesenchymal transition and fibrosis in post‐menopausal women with interstitial cystitis by targeting LPAR4 via the PI3K/Akt signaling pathway

2018 ◽  
Vol 119 (8) ◽  
pp. 6429-6441 ◽  
Author(s):  
Chen Jiang ◽  
Zhen Tong ◽  
Wei‐Lin Fang ◽  
Qi‐Bo Fu ◽  
Yin‐Jun Gu ◽  
...  
Keyword(s):  
Interstitial Cystitis ◽  
Signaling Pathway ◽  
Epithelial Mesenchymal Transition ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Mesenchymal Transition ◽  
Menopausal Women ◽  
Post Menopausal

scholarly journals Capicua homology protein inhibits the progression of gastric cancer through the PI3K/AKT signaling pathway

2020 ◽  
Author(s):  
LU GE ◽  
Chang-long Hu ◽  
Zheng-hui Ge ◽  
Chun-rong Wang ◽  
Li Qian ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Western Blot ◽  
Signaling Pathway ◽  
Cell Lines ◽  
Epithelial Mesenchymal Transition ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Mesenchymal Transition ◽  
Matrigel Invasion ◽  
Qrt Pcr

Abstract Purpose Capicua homolog protein (CIC) played a broad role in the development of cancer in humans, however, its role in the progression of gastric cancer (GC) specifically has been unclear. This study aimed to explore the expression of CIC and its potential clinical value in patients with GC. Methods The CIC levels in GC tissues and cell lines were examined by quantitative real-time polymerase chain reaction (qRT-PCR). And the in-vitro effects of CIC expression in MGC-803 cells on their proliferation, invasion, and the progression of epithelial-mesenchymal transition were assessed by CCK-8 assays, Matrigel-invasion analysis, qRT-PCR and Western blot assays, separately. In addition, the effects of downregulation of CIC on the activation of PI3K/AKT signaling pathway were measured using Western-blot analysis. Results The results showed CIC levels were lower in GC tissues and GC cell lines, and these lower CIC levels were correlated with tumor differentiation, Helicobacter pylori infection, TNM stage, and patient survival. In addition, CIC overexpression could promote cell proliferation, invasion, and progression of epithelial-mesenchymal transition in MGC-803 cells. Notably, exotic expression of CIC inactivated the phosphoinositide 3-kinase/protein kinase B signaling pathway. Conclusions In conclusion, our finding suggested CIC could serve as a potential diagnostic and prognostic biomarker and a probable therapy target for GC.

scholarly journals FERMT1 knockdown inhibits oral squamous cell carcinoma cell epithelial-mesenchymal transition by inactivating the PI3K/AKT signaling pathway

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Xiao Wang ◽  
Qianqian Chen
Keyword(s):  
Oral Cancer ◽  
Signaling Pathway ◽  
Cell Lines ◽  
Western Blotting ◽  
Epithelial Mesenchymal Transition ◽  
Akt Signaling ◽  
Migration And Invasion ◽  
Akt Signaling Pathway ◽  
Mesenchymal Transition ◽  
Tgf Β1

Abstract Background The metastasis of oral cancer is one of the main causes of death. However, the mechanisms underlying oral cancer metastasis have not been completely elucidated. Fermitin family member 1 (FERMT1) plays an -oncogene role in many cancers; however, the role of FERMT1 in oral squamous cell cancer (OSCC) remains unclear. Methods In this study, OSCC cells were treated with 5 ng/ml recombinant human Transforming growth factor-β1 (TGF-β1) protein. FERMT1 expression was measured in OSCC cell lines by RT-qPCR and western blotting. The effect of FERMT1 knockdown on the migration and invasion of OSCC cells was evaluated by Transwell assay. The epithelial-mesenchymal transition (EMT) and PI3K/AKT signaling pathway-related mRNA expression and protein levels were assessed by RT-qPCR and western blotting. Results We found that FERMT1 expression was elevated in TGF-β1-induced OSCC cell lines, and knockdown of FERMT1 inhibited the migration and invasion in TGF-β1-induced OSCC cells. FERMT1 silencing inhibited vimentin, N-cadherin, matrix metalloproteinase 9 (MMP-9) expression and promoted E-cadherin expression, suggesting that FERMT1 silencing inhibited EMT in TGF-β1-induced OSCC cells. Furthermore, FERMT1 silencing inactivated the PI3K/AKT signaling pathway in TGF-β1-induced OSCC cells. Activation of the PI3K/AKT signaling pathway reversed the effect of FERMT1 silencing on OSCC cell migration, invasion, and EMT. Conclusions FERMT1 silencing inhibits the migration, invasion, and EMT of OSCC cells via inactivation of the PI3K/AKT signaling pathway, suggesting that FERMT1 is a novel and potential therapeutic target for anti-metastatic strategies for OSCC.

microRNA-382 suppresses the progression of pancreatic cancer through the PI3K/Akt signaling pathway by inhibition of Anxa3

2020 ◽  
Vol 319 (3) ◽  
pp. G309-G322
Author(s):  
Xiaohui Wan ◽  
Dongrui Guo ◽  
Qi Zhu ◽  
Rongfeng Qu
Keyword(s):  
Pancreatic Cancer ◽  
Signaling Pathway ◽  
Epithelial Mesenchymal Transition ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Mesenchymal Transition ◽  
Node Metastasis

This study focused on the mechanism of miR-382 in epithelial mesenchymal transition and lymph node metastasis in PC in relation to Anxa3 and the PI3K/Akt signaling pathway. We found the inhibitory role of miR-382 in PC in vitro and in vivo.

scholarly journals Insulin-like Growth Factor-1-Induced Epithelial-Mesenchymal Transition Promotes Multiple Myeloma Progression

Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 5541-5541
Author(s):  
Yue Peng ◽  
Xiaman Wang ◽  
Ying Shen ◽  
Fangmei Li ◽  
Ru Zhang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Epithelial Mesenchymal Transition ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Mesenchymal Phenotype ◽  
Myeloma Cells ◽  
Mesenchymal Transition ◽  
Cell Neoplasm ◽  
D Cells ◽  
Emt Markers

MM is an incurable B cell neoplasm, which is characterized by the clonal proliferation of plasma cells in the bone marrow (BM), accounts for approximately 10% of hematological malignancies. Insulin-like growth factor-1 (IGF-1) is a vital proliferation factor in myeloma cells, recent researches demonstrated that it may be involved in MM cell metastasis. In last decade, studies have demonstrated that IGF-1 induces epithelial-mesenchymal transition (EMT), which has been tightly correlated with increased motility and invasive capacity in several cancers including gastric cancer, hepatocellular carcinoma, and melanoma. However, it remains unclear whether IGF-1 induces EMT and promote myeloma progression. In this study, we firstly observed the morphology of the myeloma cell line Karpas707 changed from tight polygon to loose spindle, a mesenchymal phenotype after treated with IGF-1 (50 ng/ml) after 72h. We supposed IGF-1 may induced EMT in myeloma cells. Furthermore, when serum-starved MM cell lines RPMI8226 and MM1.S were stimulated with 50ng/mL of IGF-1, we found that the expression of mesenchymal features was significantly upregulated in a time-dependent manner, as determined by both flow cytometry analysis and western blotting. Next we confirmed that IGF-1 can activate the PI3K/Akt signaling pathway by inducing the phosphorylation of Akt in MM cells. To investigated whether PI3K/Akt signaling pathway involved in the IGF-1 mediated EMT, we blocked PI3K/Akt signaling pathway using Akt inhibitor MK2206 in IGF-1 treated MM.1S cells. We found MK2206 reversed these changes of EMT markers. Moreover, we found the IGF-1-induced EMT promotes myeloma progression, including migration, invasion, adhesion and clone formation in MM cells, using transwell migration and invasion assay, cell adhesion assay, colony formation assay and flow cytometry. Furthermore, to further validate IGF-1-induced EMT promote MM progression, we knocked down mesenchymal marker vimentin using siRNA in MM.1S cells (VIM k/d cells). We detected that these function IGF-1 plays in myeloma was impaired in Vim k/d cells, indicating that IGF-1-induced EMT promotes MM progression. Finally, we validated that IGF1 expression is aberrantly upregulated and correlated with the expression of the EMT markers by analyzing the mRNA data of BM samples from normal donors and patients in different stages of plasma cell neoplasm from the GEO database. Taken together, these data demonstrate that the mesenchymal phenotype induced by IGF1 contributes to MM progression via PI3K/Akt pathway. Disclosures No relevant conflicts of interest to declare.

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