scholarly journals miR-146a-5p circuitry uncouples cell proliferation and migration, but not differentiation, in human mesenchymal stem cells

2013 ◽  
Vol 41 (21) ◽  
pp. 9753-9763 ◽  
Author(s):  
Jui-Yu Hsieh ◽  
Tse-Shun Huang ◽  
Shu-Meng Cheng ◽  
Wei-Shiang Lin ◽  
Tsung-Neng Tsai ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cell Proliferation ◽  
Mesenchymal Stem Cells ◽  
Human Mesenchymal Stem Cells ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals Long non-coding RNA FAM83H-AS1 induced by adipose-derived stem cells promotes breast and pancreatic cancer cell proliferation and migration

2020 ◽  
Author(s):  
Jianing Tang ◽  
Qiuxia Cui ◽  
Dan Zhang ◽  
Xing Liao ◽  
Yan Gong ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Stem Cells ◽  
Cell Proliferation ◽  
Adipose Derived Stem Cells ◽  
Unfolded Protein ◽  
Pancreatic Cancer Cells ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Protein Response ◽  
Proliferation And Migration

Abstract Background Stromal cells recruited to the tumor microenvironment and long non-coding RNAs (lncRNAs) in the tumor cells regulate cancer progression. However, their relationship is largely unknown. Methods In the current study, we identified the effects of lncRNA FAM83H-AS1, induced by adipose-derived stem cells (ADSCs) during tumor development, and explored the underlying mechanisms using a coculture cell model. Adipose tissues were obtained from healthy female donors, the expression of stromal markers on cell surface of expanded ADSCs were confirmed using immunofluorescence analysis. The breast and pancreatic cancer cells were cultured with or without ADSCs using 24-well transwell chamber systems with 8.0 µm pore size. Results Our results showed that FAM83H-AS1 was upregulated in breast and pancreatic cancers and associated with poor prognosis. ADSCs further induced FAM83H-AS1 and increased tumor cell proliferation via promoting G1/S transition through cyclin D1, CDK4 and CDK6. Wound healing, modified Boyden chamber and immunoblotting assays demonstrated that ADSCs induced epithelial-mesenchymal transition and migration of breast and pancreatic cancer cells in a FAM83H-AS1-dependent manner. And ADSC-induced FAM83H-AS1 increased unfolded protein response through AKT/XBP1 pathway. Conclusion In conclusion, our results indicated that ADSCs promoted breast and pancreatic cancer development via inducing cell proliferation and migration, as well as unfolded protein response through FAM83H-AS1.

Novel Pathway for Hypoxia-Induced Proliferation and Migration in Human Mesenchymal Stem Cells: Involvement of HIF-1α, FASN, and mTORC1

Stem Cells ◽  
2015 ◽  
Vol 33 (7) ◽  
pp. 2182-2195 ◽  
Author(s):  
Hyun Jik Lee ◽  
Jung Min Ryu ◽  
Young Hyun Jung ◽  
Sang Yub Oh ◽  
Sei-Jung Lee ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Human Mesenchymal Stem Cells ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals The Histone Demethylase KDM3B Promotes Osteo-/Odontogenic Differentiation, Cell Proliferation, and Migration Potential of Stem Cells from the Apical Papilla

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Chen Zhang ◽  
Xiao Han ◽  
Yuncun Liang ◽  
Huina Liu ◽  
Zhipeng Fan ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cell Proliferation ◽  
Histone Demethylase ◽  
Alp Activity ◽  
Cell Proliferation And Migration ◽  
Odontogenic Differentiation ◽  
Migration Potential ◽  
Apical Papilla ◽  
And Migration ◽  
Proliferation And Migration

Understanding the regulation mechanisms of mesenchymal stem cells (MSCs) can assist in tissue regeneration. The histone demethylase (KDM) family has a crucial role in differentiation and cell proliferation of MSCs, while the function of KDM3B in MSCs is not well understood. In this study, we used the stem cells from the apical papilla (SCAPs) to test whether KDM3B could regulate the function of MSCs. By an alkaline phosphatase (ALP) activity assay, Alizarin red staining, real-time RT-PCR, and western blot analysis, we found that KDM3B enhanced the ALP activity and mineralization of SCAPs and promoted the expression of runt-related transcription factor 2 (RUNX2), osterix (OSX), dentin sialophosphoprotein (DSPP), and osteocalcin (OCN). Additionally, the CFSE, CCK-8, and flow cytometry assays revealed that KDM3B improved cell proliferation by accelerating cell cycle transition from the G1 to S phase. Scratch and transwell migration assays displayed that KDM3B promoted the migration potential of SCAPs. Mechanically, microarray results displayed that 98 genes were upregulated, including STAT1, CCND1, and FGF5, and 48 genes were downregulated after KDM3B overexpression. Besides, we found that the Toll-like receptor and JAK-STAT signaling pathway may be involved in the regulating function of KDM3B in SCAPs. In brief, we discovered that KDM3B promoted the osteo-/odontogenic differentiation, cell proliferation, and migration potential of SCAPs and provided a novel target and theoretical basis for regenerative medicine.

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