MicroRNA‐4731‐5p delivered by AD‐mesenchymal stem cells induces cell cycle arrest and apoptosis in glioblastoma

2020 ◽  
Vol 235 (11) ◽  
pp. 8167-8175 ◽  
Author(s):  
Amir Allahverdi ◽  
Ehsan Arefian ◽  
Masoud Soleimani ◽  
Jafar Ai ◽  
Negin Nahanmoghaddam ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Cell Cycle Arrest ◽  
Cycle Arrest

Human bone marrow mesenchymal stem cells suppress the proliferation of hepatic stellate cells by inhibiting the ubiquitination of p27

2017 ◽  
Vol 95 (6) ◽  
pp. 628-633 ◽  
Author(s):  
Liang Wang ◽  
Guang Bai ◽  
Fei Chen
Keyword(s):  
Cell Cycle ◽  
Stem Cells ◽  
Bone Marrow ◽  
Cell Proliferation ◽  
Mesenchymal Stem Cells ◽  
Cell Cycle Arrest ◽  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
Cycle Arrest ◽  
Marrow Mesenchymal Stem Cells

Bone marrow mesenchymal stem cells (BMSCs) have considerable therapeutic potential for the treatment of end-stage liver disease. Previous studies have demonstrated that BMSCs secrete growth factors and cytokines that inactivate hepatic stellate cells (HSCs), which inhibited the progression of hepatic fibrosis. The aim of this study was to determine the mechanism by which BMSCs suppress the function of HSCs in fibrosis. Our results showed that co-culture of BMSCs and HSCs induced cell cycle arrest at the G10/G1 phase and cell apoptosis of HSCs, which finally inhibited the cell proliferation of HSCs. Consistent with the cell cycle arrest, co-culture of BMSCs and HSCs increased the abundance of the cell cycle protein p27. Mechanistically, we further uncovered that following the co-culture with BMSCs, the expression level of the E3 ligase S-phase kinase-associated protein 2 (SKP2) that is responsible for the ubiquitination of p27 was decreased, which attenuated the ubiquitination of p27 and increased the stability of p27 in HSCs. Collectively, our results indicated the potential involvement of the SKP2–p27 axis for the inhibitory effect of BSMCs on the cell proliferation of HSCs.

scholarly journals Laminar shear stress delivers cell cycle arrest and anti-apoptosis to mesenchymal stem cells

2011 ◽  
Vol 43 (3) ◽  
pp. 210-216 ◽  
Author(s):  
W. Luo ◽  
W. Xiong ◽  
J. Zhou ◽  
Z. Fang ◽  
W. Chen ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Stem Cells ◽  
Shear Stress ◽  
Mesenchymal Stem Cells ◽  
Cell Cycle Arrest ◽  
Laminar Shear Stress ◽  
Cycle Arrest ◽  
Laminar Shear

Knockdown of OY-TES-1 by RNAi causes cell cycle arrest and migration decrease in bone marrow-derived mesenchymal stem cells

2012 ◽  
Vol 36 (10) ◽  
pp. 917-922 ◽  
Author(s):  
Yan‑Hui Cen ◽  
Wen‑Wen Guo ◽  
Bin Luo ◽  
Yong‑Da Lin ◽  
Qing‑Mei Zhang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Cell Cycle Arrest ◽  
Cycle Arrest ◽  
And Migration

scholarly journals PS2 - 201 Bone Marrow-Derived Mesenchymal Stem Cells-Mediated Radioresistance in Glioma

2016 ◽  
Vol 43 (S4) ◽  
pp. S15-S15
Author(s):  
T. Zhao ◽  
G. Zadeh
Keyword(s):  
Cell Cycle ◽  
Stem Cells ◽  
Bone Marrow ◽  
Dna Damage ◽  
Mesenchymal Stem Cells ◽  
Metabolic Rate ◽  
Cell Cycle Arrest ◽  
Tumour Microenvironment ◽  
Conditioned Media ◽  
Cycle Arrest

Ionizing radiation (IR) is one of the conventional post-surgical treatments for Glioblastoma Multiforme (GBM). Mesenchymal stem cells (MSCs) constitute a subpopulation of bone marrow derived cells which are actively recruited to the site of radiation and/or tumour microenvironment (TME), both of which have important implications for neovascularization and tumor progression. The goal of this project is to investigate the functional contribution of MSCs in the TME. We postulate that Bone Marrow-MSCs promote radio-resistance in GBM via cell cycle arrest. We tested the effect of MSC on U87 glioblastoma cell line in response to IR. We found that MSC co-culture, MSC-conditioned media (MSCCM) and irradiated MSC-conditioned media (MSCIRCM) did not reduce IR-induced p53 (ser15) phosphorylation, signifying intact p53-dependent DNA damage pathway in all conditions. However, both MSCCM and MSCIRCM temporally increased phospho-Chk2, a kinase involved in ATM-dependent cascade and cell cycle arrest. This increase occurred at 24 hours and reverted to baseline levels by 48 hours. Interestingly, IR (15Gy) caused transiently heightened metabolic rate under MSC and MSC IRCM as opposed to IR-null treatment at 48 hours elevated cell proliferation. MSCCM, but not MSCIRCM, marginally reduced caspase 3/7-dependent apoptotic levels. The combination of IR and MSCCM as well as MSCIRCM first increased protein level of phospho-Chk2 at 24 hours; followed by increased metabolic rate at 48 hours; and lastly, boosted proliferation at 72 hours. This data combined proposes plausible machinery for BM-MSC mediated radio-resistance by initiating cell cycle arrest in tumour cells for DNA damage repair.

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