scholarly journals GATA1 gene silencing inhibits invasion, proliferation and migration of cholangiocarcinoma stem cells via disrupting the PI3K/AKT pathway

2019 ◽  
Vol Volume 12 ◽  
pp. 5335-5354 ◽  
Author(s):  
Guang Shi ◽  
Hong Zhang ◽  
Qiong Yu ◽  
Chunmei Hu ◽  
Youbo Ji
Keyword(s):  
Stem Cells ◽  
Gene Silencing ◽  
Akt Pathway ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals Paracrine Interleukin-8 affects mesenchymal stem cells through the Akt pathway and enhances human umbilical vein endothelial cell proliferation and migration

2021 ◽  
Author(s):  
Lulu wang ◽  
Yongtao Li ◽  
Xiaodong Zhang ◽  
Na Liu ◽  
Shiyang Shen ◽  
...  
Keyword(s):  
Stem Cells ◽  
Endothelial Cells ◽  
Mesenchymal Stem Cells ◽  
High Glucose ◽  
Umbilical Vein ◽  
Interleukin 8 ◽  
Akt Pathway ◽  
Human Umbilical Vein ◽  
And Migration ◽  
Proliferation And Migration

Interleukin-8 (IL-8) promotes cell homing and angiogenesis, but its effects on activating human bone marrow mesenchymal stem cells (BMSCs) and promoting angiogenesis are unclear. We used bioinformatics to predict these processes. In vitro, BMSCs were stimulated in a high-glucose (HG) environment with 50 μg/mL or 100 μg/mL IL-8 were used as the IL-8 group. 5μmol/L Triciribine was added to the two IL-8 groups as the Akt inhibitor group. Cultured human umbilical vein endothelial cells (HUVECs) were cultured in BMSCs conditioned medium (CM). Observe the changes in proliferation, apoptosis, migration ability and levels of VEGF and IL-6 in HUVEC each group. 70 processes and 26 pathways were involved in vascular development, through which IL-8 affected BMSCs. Compared with the high-glucose control group, HUVEC proliferation A value, Gap closure rate, and Transwell cell migration rate in the IL-8 50 and IL-8 100 CM groups were significantly increased (P<0.01, n=30). However, HUVEC apoptosis was significantly decreased (P<0.01, n=30). Akt and phospho-Akt protein contents in lysates of BMSCs treated with IL-8, as well as VEGF and IL-6 protein contents in the supernatant of BMSCs treated with IL-8, were all highly expressed (P<0.01, n=15). These analyses confirmed that IL-8 promoted the expression of 41 core proteins in BMSCs through the PI3K Akt pathway, which could promote the proliferation and migration of vascular endothelial cells. Therefore, in a high-glucose environment, IL-8 activated the Akt signaling pathway, promoted paracrine mechanisms of BMSCs, and improved the proliferation and migration of HUVECs.

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.

scholarly journals Effects of RNAi-mediated MUC4 gene silencing on the proliferation and migration of human pancreatic carcinoma BxPC-3 cells

2016 ◽  
Vol 36 (6) ◽  
pp. 3449-3455 ◽  
Author(s):  
Yong Li ◽  
Changqiang Wu ◽  
Tianwu Chen ◽  
Juanjuan Zhang ◽  
Gang Liu ◽  
...  
Keyword(s):  
Gene Silencing ◽  
Pancreatic Carcinoma ◽  
And Migration ◽  
Muc4 Gene ◽  
Proliferation And Migration
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