scholarly journals UNBS5162 and amonafide inhibits tumor progression in human melanoma by the AKT/mTOR pathway

2019 ◽  
Vol Volume 11 ◽  
pp. 2339-2348
Author(s):  
Yingyi Ye ◽  
Shuhong Huang ◽  
Yingying Wu
Keyword(s):  
Tumor Progression ◽  
Human Melanoma ◽  
Mtor Pathway

Exogenous hydrogen sulfide inhibits human melanoma cell development via suppression of the PI3K/AKT/ mTOR pathway

2020 ◽  
Vol 98 (1) ◽  
pp. 26-34 ◽  
Author(s):  
Qing Xiao ◽  
Jiayi Ying ◽  
Zhuhui Qiao ◽  
Yiwen Yang ◽  
Xiaoxi Dai ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Melanoma Cell ◽  
Cell Development ◽  
Human Melanoma ◽  
Mtor Pathway ◽  
Human Melanoma Cell

VEGF and Tumor Progression in Human Melanoma

2004 ◽  
pp. 48-53 ◽  
Author(s):  
Domenico Ribatti ◽  
Angelo Vacca ◽  
Franco Dammacco
Keyword(s):  
Tumor Progression ◽  
Human Melanoma

scholarly journals The downregulation of type I IFN signaling in G-MDSCs under tumor conditions promotes their development towards an immunosuppressive phenotype

2022 ◽  
Vol 13 (1) ◽  
Author(s):  
Yingying Sun ◽  
Xiaoqing Han ◽  
Chao Shang ◽  
Yawei Wang ◽  
Boya Xu ◽  
...  
Keyword(s):  
Tumor Progression ◽  
Suppressor Cells ◽  
Myeloid Cell ◽  
Mtor Pathway ◽  
Mouse Serum ◽  
Cytokine Signaling ◽  
Type I ◽  
Myeloid Derived Suppressor Cells ◽  
Immunosuppressive Microenvironment ◽  
Normal Differentiation

AbstractTumors modify myeloid cell differentiation and induce an immunosuppressive microenvironment. Granulocytic myeloid-derived suppressor cells (G-MDSCs), the main subgroup of myeloid-derived suppressor cells (MDSCs), are immature myeloid cells (IMCs) with immunosuppressive activity and exist in tumor-bearing hosts. The reason why these cells diverge from a normal differentiation pathway and are shaped into immunosuppressive cells remains unclear. Here, we reported that the increase of granulocyte colony-stimulating factor (G-CSF) in mouse serum with tumor progression encouraged G-MDSCs to obtain immunosuppressive traits in peripheral blood through the PI3K-Akt/mTOR pathway. Importantly, we found that downregulation of type I interferon (IFN-I) signaling in G-MDSCs was a prerequisite for their immunosuppressive effects. Suppressor of cytokine signaling (SOCS1), the action of which is dependent on IFN-I signaling, inhibited the activation of the PI3K-Akt/mTOR pathway by directly interacting with Akt, indicating that the differentiation of immunosuppressive G-MDSCs involves a transition from immune activation to immune tolerance. Our study suggests that increasing IFN-I signaling in G-MDSCs may be a strategy for reprograming immunosuppressive myelopoiesis and slowing tumor progression.

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