Effects of FOSL1 silencing on osteosarcoma cell proliferation, invasion and migration through the ERK/AP-1 signaling pathway

2018 ◽  
Vol 234 (4) ◽  
pp. 3598-3612 ◽  
Author(s):  
Yu Han ◽  
Xingyu Zhao ◽  
Yifu Sun ◽  
Yutong Sui ◽  
Jianguo Liu
Keyword(s):  
Cell Proliferation ◽  
Signaling Pathway ◽  
Osteosarcoma Cell ◽  
Invasion And Migration ◽  
And Migration

miR-340 Inhibits the Development of Hepatocellular Carcinoma by Down-Regulating Akt Signaling Pathway

2021 ◽  
Vol 11 (9) ◽  
pp. 1785-1791
Author(s):  
Tangpeng Xu ◽  
Changli Ruan ◽  
Xu Bin ◽  
Mengxue Hu
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Pathological Grade ◽  
Akt Signaling Pathway ◽  
Invasion And Migration ◽  
Proliferation Ability ◽  
And Migration ◽  
Cancer Tissues

Hepatocellular carcinoma (HCC) is a serious threat to human health. miR-340 participates in HCC pathogenesis, but its specific mechanism is not completely clear. Therefore, our study assessed the mechanism by how miR-340 involves in HCC. The cancer tissues and paracancerous tissues of HCC patients were collected. miR-340 mimics/NC and Akt siRNA were transfected into HepG2 cells followed by analysis of miR-304 and EMT-related molecules expression by Real-time PCR, cell invasion and migration by Transwell assay, cell proliferation ability by CCK8 assay as well as p-Akt and p-mTOR level by Western blot. miR-340 in HCC tissues was significantly downregulated compared to adjacent tissues (P <0.001). With increased pathological grade, miR-340 expression was decreased gradually. p-Akt and p-mTOR in HCC tissues was significantly upregulated and elevated gradually with increased pathological grade. p-Akt and p-mTOR was negatively associated with miR-340 (P <0.001). After overexpression of miR-340, HepG2 cell proliferation, invasion, migration and epithelialization were significantly inhibited, and p-Akt and p-mTOR was reduced. When Akt expression was interfered with siRNA, cell proliferation and epithelialization was further inhibited. miR-340 inhibits the development of hepatocellular carcinoma through Akt signaling pathway.

scholarly journals LncRNA BE503655 inhibits osteosarcoma cell proliferation, invasion/migration via Wnt/β-catenin pathway

2019 ◽  
Vol 39 (7) ◽  
Author(s):  
Qiang Huang ◽  
Shu-yan Shi ◽  
Hai-bo Ji ◽  
Shu-xing Xing
Keyword(s):  
Cell Proliferation ◽  
Histological Grade ◽  
Osteosarcoma Cell ◽  
Rna Seq ◽  
Invasion And Migration ◽  
Non Coding Rnas ◽  
And Migration ◽  
Enneking Stage ◽  
The Relationship

Abstract Aim: In previous studies, numerous dysregulated long non-coding RNAs (lncRNAs) were identified by RNA-sequencing (RNA-seq). However, the relationship between lncRNA and osteosarcoma remains unclear. In the present study, the function and mechanism of lncRNA BE503655 were investigated. Methods: Transwell, cell cycle and proliferation were used to evaluate the function of lncRNA BE503655. Real-time PCR and Western blotting were used to detect the expression of lncRNA BE503655 and β-catenin. Results: LncRNA BE503655 is overexpressed in human osteosarcoma and osteosarcoma cell lines. Knockdown lncRNA BE503655 suppresses cell proliferation, invasion and migration. High expression of BE503655 was significantly related to Enneking stage, distant metastasis and histological grade. Moreover, we also provided evidences that lncRNA BE503655 played its functions dependent on regulation of Wnt/β-catenin signaling in osteosarcoma. Conclusion: Taken together, we verified the role of lncRNA BE503655 and provided possible mechanism in osteosarcoma. Our study provided new insights into clinical treatment of osteosarcoma and further intervention target.

scholarly journals Aldolase A Promotes Proliferation and Metastasis of Colorectal Cancer through Targeting COPS6 and Regulating MAPK Signaling Pathway

2021 ◽  
Author(s):  
Ya Lu ◽  
Yuan Zhang ◽  
Hui Zhang ◽  
Yue Zhu ◽  
Junying Zhang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Signaling Pathway ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Invasion And Migration ◽  
Proliferation And Metastasis ◽  
And Migration ◽  
Aldolase A

Abstract Background: Colorectal cancer (CRC) is a serious threat to human health, and its underlying mechanisms needs further explored. Aldolase A (ALDOA) has received increasing attention for its reported association with multiple cancers, but the function and mechanism of ALDOA in CRC remain unclear. We aimed to evaluate the biological role of ALDOA in CRC.Methods: The stable ALDOA knockdown or overexpression cell lines were established for subsequent experiments. The qRT-PCR and western blotting were used to detect the expression of ALDOA and COPS6 and the relative protein levels of epithelial-mesenchymal transition (EMT) and MAPK signaling pathway. Immunofluorescence (IF) assay was applied to determine ALDOA localization. CCK-8, transwell, and wound healing assays were performed to evaluate CRC cell proliferation, invasion, and migration. Mouse xenograft models were established to verify the effect of ALDOA on CRC cell growth in vivo. Immunoprecipitation (IP) assay and mass spectrometry (MS) analysis were conducted to identify the interactions between ALDOA and COPS6.Results: ALDOA was overexpressed in CRC tissues and cell lines. Silencing ALDOA significantly impaired the proliferation, invasion and migration of CRC cells in vitro, and obviously decreased the growth of CRC cells in vivo. Mechanically, ALDOA bound to and regulated COPS6, and the promoting effects of upregulated ALDOA on CRC cell proliferation and metastasis were inhibited by the depletion of COPS6. Besides, EMT program and MAPK signaling pathway were activated by ALDOA overexpression.Conclusion: ALDOA facilitated the proliferation, invasion and migration of CRC through binding and regulating COPS6, inducing EMT and activating MAPK signaling pathway.

Bone Marrow Mesenchymal Stem Cells (BMSC)-Derived MicroRNA-189 Inhibits Glioma Tumorigenesis Through Suppressing Tumor Necrosis Factor-α (TNF-α)-Mediated Nuclear Factor Kappa Light Chain Enhancer of Activated B Cells (NF-κB) Signaling Pathway

2022 ◽  
Vol 12 (3) ◽  
pp. 581-587
Author(s):  
Wenxu Rao ◽  
Kang Yin
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Cell Proliferation ◽  
Mesenchymal Stem Cells ◽  
Signaling Pathway ◽  
Inflammatory Factors ◽  
Invasion And Migration ◽  
Marrow Mesenchymal Stem Cells ◽  
And Migration

This study aims at investigating the mechanism underlying bone marrow mesenchymal stem cells (BMSC) function in glioma. Glioma cells were administered with plasmids loading NF-κB siRNA, microRNA (miRNA)-189 inhibitor, or miR-189 mimics for transfection followed by analysis of miR-189 expression by RT-qPCR, cell apoptosis by flow cytometry, cell proliferation by MTT assay,invasion and migration by Transwell assay, inflammatory factors secretion by ELISA as well as proteins expression by western blot. A mouse model of glioma was established to detect the in vivo effect of BMSCs. miR-189 was lowly expressed in glioma cell lines but enriched in BMSCs. When miR-189 was silenced, cell proliferation, invasion and migration were potentiated and apoptosis was decreased, along with enhancement of N-cadherin, Vimentin, MMP-2 and and MMP-9, and decline in Bax, cleaved casepase-3 and cleaved PARP. Silencing of NF-κB reversed the effect of miR-189 inhibitor on cell progression, accompanied with reduction of inflammatory factors. BMSCs treatment effectively promoted miR-189 expression in glioma and inactivated TNF-α/NF-κB signaling, thereby suppressing tumor growth. In conclusion, miR-189 derived from BMSC inhibits glioma progression through regulation of TNF-α/NF-κB signaling pathway.

scholarly journals Circ-SOX4 drives the tumorigenesis and development of lung adenocarcinoma via sponging miR-1270 and modulating PLAGL2 to activate WNT signaling pathway

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Nan Gao ◽  
Baoguo Ye
Keyword(s):  
Cell Proliferation ◽  
Lung Adenocarcinoma ◽  
Wnt Signaling ◽  
Signaling Pathway ◽  
Molecular Mechanism ◽  
Biological Function ◽  
Wnt Signaling Pathway ◽  
Luciferase Reporter ◽  
Invasion And Migration ◽  
And Migration

Abstract Background Lung adenocarcinoma (LUAD), a widespread histopathological subtype of lung cancer, is deemed as a malignant tumor with a peak risk of mortality. Emerged as RNA with a loop structure that depleted protein coding ability, circular RNA (circRNA) has been identified as a regulator in cancer progression. Circ-SOX4, identified as a novel circRNA, has not been studied in any cancer yet. Thus, the regulatory function that circ-SOX4 exerts on LUAD development remains obscure. Aim of the study This study aimed to investigate the biological function and molecular mechanism of circ-SOX4 in LUAD. Methods The expression of circ-SOX4 was detected by qRT-PCR. CCK-8, colony formation, transwell and wound healing assays were performed to explore the biological function of circ-SOX4 in LUAD. The interaction between miR-1270 and circ-SOX41 (or PLAGL2) was confirmed by RNA pull down, luciferase reporter and RIP assays. Results Circ-SOX4 was found to be obviously upregulated in LUAD tissues and cells, and knockdown of it inhibited cell proliferation, invasion and migration in LUAD. Furthermore, silenced circ-SOX4 also inhibited LUAD tumor growth. Molecular mechanism assays revealed that circ-SOX4 interacted with miR-1270 in LUAD. Besides, PLAGL2 was confirmed as a downstream gene of miR-1270. Rescue assays validated that miR-1270 suppression or PLAGL2 overexpression countervailed circ-SOX4 depletion-mediated inhibition on cell proliferation, invasion and migration in LUAD. Additionally, it was discovered that circ-SOX4/miR-1270/PLAGL2 axis activated WNT signaling pathway in LUAD. Conclusions Circ-SOX4 boosted the development of LUAD and activate WNT signaling pathway through sponging miR-1270 and modulating PLAGL2, which provided a valuable theoretical basis for exploring underlying therapeutic target in LUAD.

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