scholarly journals Co-culture with lung cancer A549 cells promotes the proliferation and migration of mesenchymal stem cells derived from bone marrow

2017 ◽  
Vol 14 (4) ◽  
pp. 2983-2991 ◽  
Author(s):  
Yue-Mei Zhang ◽  
Zhi-Ming Zhang ◽  
Quan-Lin Guan ◽  
Yong-Qi Liu ◽  
Zhi-Wei Wu ◽  
...  
2022 ◽  
Vol 12 (3) ◽  
pp. 597-601
Author(s):  
Haibin Song ◽  
Heng Zhang ◽  
Lei Li

Deriving from bone marrow, the bone marrow mesenchymal stem cells (BMSCs) possess multipolar chemotaxis, proliferation potential, along with the capability to differentiate into various types of cells. Moreover, the hypoxic stimulation can effectively induce BMSCs differentiation. This study intends to explore the impediment of BMSCs on malignant behaviors of lung cancer stem cells under hypoxia. A co-culture system of BMSCs with A549 cells was established and then assigned into normoxia group, hypoxia group (50, 100, and 200 nmol/L) followed by analysis of cell viability by CCK-8 assay and miR-145 expression by qRT-PCR. In addition, A549 cells were grouped into NC group, miR-145-mimics group, and miR-145-inhibitors group followed by analysis of cell invasion and levels of miR-145 and Oct4. Hypoxia group exhibited a reduced cell viability and higher miR-145 expression (146.01±21.23%) compared to normoxia group (P < 0.05). Transfection of miR-145-mimic significantly upregulated miR-145 and decreased cell invasion (7.49±1.43%) compared with miR-145-inhibitors group or NC group (P < 0.05). Meanwhile, Oct4 level in miR-145-mimics group (0.934±2.98) was significantly decreased (P < 0.05). In conclusion, under hypoxia condition, the co-culture with BMSCs can upregulated miR-145 level, effectively reduce the viability of lung cancer stem cells and restrain proliferation capability.


2021 ◽  
Vol 11 (12) ◽  
pp. 2357-2366
Author(s):  
Xiaopeng Guo ◽  
Yingsong Liu ◽  
Mingzhu Wei

We aimed to explore the mechanism by how LX4211 affects bone marrow mesenchymal stem cells (BMSCs) during ischemia-reperfusion (I/R). BMSCs were extracted and treated with LX4211 followed by analysis of cell proliferation and migration by CCK-8, Transwell assay and wound healing tests, cell apoptosis and cycle by flow cytometry, exosomes and VEGFA secretion by immunoenzyme-linked adsorption. BMSCs treated with LX4211 or DMSO were administrated into mice with blood perfusion and capillary or arteriolar density was detected. Treatment with LX4211 significantly inhibited BMSCs proliferation, increased apoptosis and activated AMPK/ACC signaling along with reduced the number of exosomes and VEGFA level and impaired physiological functions. In vivo experiments determined that LX4211 alleviated I/R of lower limbs by inhibiting the muscle retention of BMSCs and paracrine. In conclusion, LX4211 treatment can delay the blood recovery of ischemic non-diabetic mice by reducing the proliferation, migration and impairing paracrine of BMSCs.


2017 ◽  
Vol 39 (11) ◽  
pp. 1649-1655 ◽  
Author(s):  
Wumei Yuan ◽  
Lijuan Cui ◽  
Guoxiang Li ◽  
Na Wang ◽  
Pan Zhang ◽  
...  

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Anh Thi Mai Nguyen ◽  
Ha Le Bao Tran ◽  
Thuy Anh Vu Pham

Objective. To access the effects of platelet-rich plasma (PRP) on the behaviour of human bone marrow-derived mesenchymal stem cells (hBMSCs), including proliferation and migration. Methods. PRP was diluted with DMEM/F12, resulting in concentrations of 1%, 2%, and 5%. The proliferation of hBMSCs was examined by 2 methods: cell-number counting with the haemocytometer method and the colony-forming unit-fibroblast (CFU-F) assay. Cell migration was evaluated using the scratch wound healing (SWH) assay; after that, the recorded digital images were analysed by the Image-Analysis J 1.51j8 software to compare the cell-free areas between groups after 0, 24, and 48 hours. Results. hBMSCs cultured in DMEM/F12 at PRP concentrations of 1%, 2%, and 5% were all able to proliferate and migrate. In the 5% PRP group, hBMSCs proliferated greatly with a significantly higher cell number than reported for all other groups on days 5, 7, and 9. CFU-Fs were observed in all groups, except for the negative control group. The SWH assay demonstrated that hBMSCs cultured in 2% and 5% PRP almost filled the artificial wound scratch and significantly migrated more than those of all other groups at both 24 h and 48 h. Conclusion. This study indicated that, due to the significant enhancement of cell proliferation and migration, 5% PRP might be the optimal concentration that should be used to promote the potential of hBMSCs in wound healing.


2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Weidong Ma ◽  
Ziyuan Wang ◽  
Yan Zhao ◽  
Qibin Wang ◽  
Yonghong Zhang ◽  
...  

Inflammatory reactions mediated by the NACHT, LRR, and PYD domain-containing protein 3 (NLRP3) inflammasome contributes to non-small-cell lung cancer (NSCLC) progression, particularly in patients with bacterial infections. Salidroside (SAL) has recently been shown to suppress lipopolysaccharide- (LPS-) induced NSCLC proliferation and migration, but its mechanism of action remains unclear. It has been shown that SAL improves metabolic inflammation in diabetic rodents through AMP-activated protein kinase- (AMPK-) dependent inhibition of the NLRP3 inflammasome. However, whether the NLRP3 inflammasome is regulated by SAL in NSCLC cells and how its underlying mechanism(s) can be determined require clarification. In this study, human lung alveolar basal carcinoma epithelial (A549) cells were treated with LPS, and the effects of SAL on cell proliferation, migration, AMPK activity, reactive oxygen species (ROS) production, and NLRP3 inflammasome activation were investigated. We found that LPS induction increases the proliferation and migration of A549 cells which was suppressed by SAL. Moreover, SAL protected A549 cells against LPS-induced AMPK inhibition, ROS production, and NLRP3 inflammasome activation. Blocking AMPK using Compound C almost completely suppressed the beneficial effects of SAL. In summary, these results indicate that SAL suppresses the proliferation and migration of human lung cancer cells through AMPK-dependent NLRP3 inflammasome regulation.


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