scholarly journals Decrease in stathmin expression by arsenic trioxide inhibits the proliferation and invasion of osteosarcoma cells via the MAPK signal pathway

2017 ◽  
Vol 14 (2) ◽  
pp. 1333-1340 ◽  
Author(s):  
Tao Feng ◽  
Jun Xu ◽  
Ping He ◽  
Yuanyuan Chen ◽  
Ruiying Fang ◽  
...  
Keyword(s):  
Arsenic Trioxide ◽  
Signal Pathway ◽  
Osteosarcoma Cells ◽  
Mapk Signal Pathway ◽  
Proliferation And Invasion

scholarly journals SPAK-p38 MAPK signal pathway modulates claudin-18 and barrier function of alveolar epithelium after hyperoxic exposure

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Chih-Hao Shen ◽  
Jr-Yu Lin ◽  
Cheng-Yo Lu ◽  
Sung-Sen Yang ◽  
Chung-Kan Peng ◽  
...  
Keyword(s):  
P38 Mapk ◽  
Knockout Mice ◽  
Barrier Function ◽  
Alveolar Epithelium ◽  
Signal Pathway ◽  
Control Group ◽  
Barrier Dysfunction ◽  
Hyperoxic Exposure ◽  
Monolayer Permeability ◽  
Mapk Signal Pathway

Abstract Background Hyperoxia downregulates the tight junction (TJ) proteins of the alveolar epithelium and leads to barrier dysfunction. Previous study has showed that STE20/SPS1-related proline/alanine-rich kinase (SPAK) interferes with the intestinal barrier function in mice. The aim of the present study is to explore the association between SPAK and barrier function in the alveolar epithelium after hyperoxic exposure. Methods Hyperoxic acute lung injury (HALI) was induced by exposing mice to > 99% oxygen for 64 h. The mice were randomly allotted into four groups comprising two control groups and two hyperoxic groups with and without SPAK knockout. Mouse alveolar MLE-12 cells were cultured in control and hyperoxic conditions with or without SPAK knockdown. Transepithelial electric resistance and transwell monolayer permeability were measured for each group. In-cell western assay was used to screen the possible mechanism of p-SPAK being induced by hyperoxia. Results Compared with the control group, SPAK knockout mice had a lower protein level in the bronchoalveolar lavage fluid in HALI, which was correlated with a lower extent of TJ disruption according to transmission electron microscopy. Hyperoxia down-regulated claudin-18 in the alveolar epithelium, which was alleviated in SPAK knockout mice. In MLE-12 cells, hyperoxia up-regulated phosphorylated-SPAK by reactive oxygen species (ROS), which was inhibited by indomethacin. Compared with the control group, SPAK knockdown MLE-12 cells had higher transepithelial electrical resistance and lower transwell monolayer permeability after hyperoxic exposure. The expression of claudin-18 was suppressed by hyperoxia, and down-regulation of SPAK restored the expression of claudin-18. The process of SPAK suppressing the expression of claudin-18 and impairing the barrier function was mediated by p38 mitogen-activated protein kinase (MAPK). Conclusions Hyperoxia up-regulates the SPAK-p38 MAPK signal pathway by ROS, which disrupts the TJ of the alveolar epithelium by suppressing the expression of claudin-18. The down-regulation of SPAK attenuates this process and protects the alveolar epithelium against the barrier dysfunction induced by hyperoxia.

Effect of silencing NEK2 on biological behaviors of HepG2 in human hepatoma cells and MAPK signal pathway

Tumor Biology ◽  
2015 ◽  
Vol 37 (2) ◽  
pp. 2023-2035 ◽  
Author(s):  
Mei-Xia Zhang ◽  
Xi-Ming Xu ◽  
Peng Zhang ◽  
Na-Na Han ◽  
Jun-Jian Deng ◽  
...  
Keyword(s):  
Hepatoma Cells ◽  
Signal Pathway ◽  
Human Hepatoma ◽  
Human Hepatoma Cells ◽  
Mapk Signal Pathway

scholarly journals Inhibition of Skp2 suppresses the proliferation and invasion of osteosarcoma cells

2017 ◽  
Vol 38 (2) ◽  
pp. 933-940 ◽  
Author(s):  
Lu Ding ◽  
Rong Li ◽  
Xiaoping Han ◽  
Yubo Zhou ◽  
Hua Zhang ◽  
...  
Keyword(s):  
Osteosarcoma Cells ◽  
Proliferation And Invasion

LncRNA GAS5 suppresses the proliferation and invasion of osteosarcoma cells via the miR-23a-3p/PTEN/PI3K/AKT pathway

2020 ◽  
Author(s):  
Jianmin Liu ◽  
Ming Chen ◽  
Longyang Ma ◽  
Xingbo Dang ◽  
Gongliang Du
Keyword(s):  
Tumor Suppressor ◽  
Tumor Growth ◽  
Akt Pathway ◽  
Osteosarcoma Cell ◽  
Osteosarcoma Cells ◽  
Cell Behaviors ◽  
Human Osteosarcoma ◽  
Proliferation And Invasion

Abstract Background: Accumulating evidence has shown that lncRNA growth arrest special 5 (GAS5) is a well‑known tumor suppressor in the pathogenesis of a variety of human cancers. However, the detailed role of GAS5 in osteosarcoma is largely unclear. Here, we explore the role of GAS5 in progression of osteosarcoma. Methods: The expression level of GAS5 was detected in human osteosarcoma tissues and matched adjacent tissues, as well as osteosarcoma cell lines and non-malignant osteoblast cells. Then, in vitro gain- and loss-of-function experiments, with the pcDNA-GAS5 expression vector and GAS5-siRNA, were performed in U2OS and HOS cells to determine the effect of GAS5 on osteosarcoma cell proliferation and invasion. Subsequently, we searched potential miRNA targets with bioinformatics analysis and confirmed their interaction by using luciferase reporter gene and RNA pull-down assays. The function and mechanism of miR-23a-3p in proliferation and invasion was also investigated in U2OS and HOS cells. Furthermore, rescue experiments were performed to verify the involvement of miR-23a-3p and its target gene in GAS5-mediated cell behaviors. Finally, a xenograft nude mouse model was established by subcutaneous injection with U2OS cells overexpressing GAS5 or not, and the effect of GAS5 on tumor growth in vivo was evaluated. Results: GAS5 was downregulated in human osteosarcoma tissues and cell lines. Overexpression of GAS5 could significantly suppress, and downregulation of GAS5 promoted, proliferation and invasion of osteosarcoma cells. GAS5 could directly bind with and downregulated miR-23a-3p that post-transcriptionally downregulated the tumor suppressor PTEN and positively regulated proliferation and invasion of osteosarcoma cells. Rescue experiments confirmed the involvement of miR-23a-3p and PTEN in GAS5-mediated cell behaviors by modifying the phosphatidylinositol-3-kinases/protein-serine-threonine kinase (PI3K/AKT) pathway. GAS5 could inhibit tumor growth in vivo . Conclusion: GAS5 functions as a competing endogenous RNA , sponging miR-23a-3p, to promote PTEN expression and suppress cell growth and invasion in osteosarcoma by regulating the PI3K/AKT pathway.

scholarly journals NOX4/ROS mediate ethanol‑induced apoptosis via MAPK signal pathway in L‑02 cells

2018 ◽  
Author(s):  
Cheng‑Fang Yang ◽  
Yu‑Juan Zhong ◽  
Zuheng Ma ◽  
Li Li ◽  
Lin Shi ◽  
...  
Keyword(s):  
Signal Pathway ◽  
Induced Apoptosis ◽  
Mapk Signal Pathway

scholarly journals Histidine‐rich glycoprotein ameliorates endothelial barrier dysfunction through regulation of NF‐κB and MAPK signal pathway

2019 ◽  
Vol 176 (15) ◽  
pp. 2808-2824 ◽  
Author(s):  
Shangze Gao ◽  
Hidenori Wake ◽  
Yuan Gao ◽  
Dengli Wang ◽  
Shuji Mori ◽  
...  
Keyword(s):  
Signal Pathway ◽  
Endothelial Barrier ◽  
Barrier Dysfunction ◽  
Endothelial Barrier Dysfunction ◽  
Mapk Signal Pathway

scholarly journals Effects of Titanium Micro-Nanopermeable Structures on Osteogenic Differentiation

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Jiannan Liu ◽  
Mingjiang Jin ◽  
Zhen Zhang ◽  
Lihuang Wu ◽  
Xuejun Jin ◽  
...  
Keyword(s):  
Osteoblast Differentiation ◽  
Signal Pathway ◽  
Acid Etching ◽  
Porous Structures ◽  
Osteoblast Proliferation ◽  
Activity Assay ◽  
Alp Activity ◽  
Erk Phosphorylation ◽  
Proliferation And Differentiation ◽  
Mapk Signal Pathway

To evaluate the effects of different Ti surface micro-nanopermeable structures on osteoblast proliferation and differentiation and explore related mechanisms, hybrid technology of sandblast, acid etching, and hydrothermal (HT) was used to form the micro-nanopermeable surface of Ti. Scanning electron microscopy (SEM), surface profiler, and contact angle meter were utilized to assess the surface morphology, roughness, and hydrophilicity. MTT, SEM, alkaline phosphatase (ALP) activity assay, and real-time PCR were performed to investigate proliferation, adhesion and spreading, and differentiation of MC3T3-E1 cells grown on polished Ti (control), sandblast + acid etching- (SLA-) treated Ti, and SLA + HT-treated Ti. MAPK signal pathway activity was evaluated by Western blotting. The results showed that SLA + HT could result in not only formation of microscale groove containing submicroscale and nanoscale porous structures in Ti samples but also rough and hydrophilic surface. SLA + HT treatment has the best effects on cell adhesion and spreading. Significantly increased levels of ALP activity and osteogenic genes including Alp, Ocn, Opn, Runx2, and Bsp, as well as p38 but not ERK phosphorylation, were found in the SLA + HT group. In conclusion, sandblast, acid etching, and hydrothermal treatment on Ti regulates osteoblast differentiation, while activation of the MAPK p38 signaling pathway served as the mechanism.

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