Chitosan Oligosaccharides Inhibit Tumor Progression and Induce Autophagy Through Activation of the p53/mTOR Pathway in Osteosarcoma

2019 ◽  
Author(s):  
Zhen Pan ◽  
Xiao-juan Wei ◽  
Shi-jie Li ◽  
Hua Guo ◽  
Dong-dong Cheng ◽  
...  
Keyword(s):  
Tumor Progression ◽  
Mtor Pathway ◽  
Chitosan Oligosaccharides

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

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.

Chitooligosaccharides inhibit tumor progression and induce autophagy through the activation of the p53/mTOR pathway in osteosarcoma

2021 ◽  
Vol 258 ◽  
pp. 117596
Author(s):  
Zhen Pan ◽  
Dong-dong Cheng ◽  
Xiao-juan Wei ◽  
Shi-jie Li ◽  
Hua Guo ◽  
...  
Keyword(s):  
Tumor Progression ◽  
Mtor Pathway

scholarly journals Cholesteryl Ester Promotes Mammary Tumor Growth in MMTV-PyMT Mice and Activates Akt-mTOR Pathway in Tumor Cells

Biomolecules ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 853
Author(s):  
Lengyun Wei ◽  
Xuyang Lu ◽  
Shengmei Weng ◽  
Shenglong Zhu ◽  
Yongquan Chen
Keyword(s):  
Tumor Growth ◽  
Cholesteryl Ester ◽  
Tumor Progression ◽  
Mammary Tumor ◽  
Causal Effect ◽  
Mtor Pathway ◽  
Breast Tumor Cell ◽  
Mammary Tumor Growth ◽  
Mammary Tumor Progression ◽  
Mcf 7

The association between intratumoral cholesteryl ester (CE) and tumor progression has been reported previously. The objective of our study was to investigate a causal effect of CE on mammary tumor progression. Using MMTV-PyMT (MMTV-polyoma virus middle T) transgenic mice and breast tumor cell MCF-7, we show that both exogenous and endogenous CE can increase mammary tumor growth, that CE upregulates the AKT/mTOR pathway, and that CE synthesis blockade suppresses this signaling pathway. Our data suggest that SOAT1, a sterol O-acyltransferase, may be a potential target for the treatment of breast cancer.

scholarly journals Mammalian target of rapamycin inhibition abrogates insulin-mediated mammary tumor progression in type 2 diabetes

2010 ◽  
Vol 17 (4) ◽  
pp. 941-951 ◽  
Author(s):  
Yvonne Fierz ◽  
Ruslan Novosyadlyy ◽  
Archana Vijayakumar ◽  
Shoshana Yakar ◽  
Derek LeRoith
Keyword(s):  
Breast Cancer ◽  
Type 2 Diabetes ◽  
Tumor Growth ◽  
Tumor Progression ◽  
Mammary Tumor ◽  
Mammalian Target Of Rapamycin ◽  
Mtor Pathway ◽  
Mtor Inhibition ◽  
Mammary Tumor Progression

Type 2 diabetes increases breast cancer risk and mortality, and hyperinsulinemia is a major mediator of this effect. The mammalian target of rapamycin (mTOR) is activated by insulin and is a key regulator of mammary tumor progression. Pharmacological mTOR inhibition suppresses tumor growth in numerous mammary tumor models in the non-diabetic setting. However, the role of the mTOR pathway in type 2 diabetes-induced tumor growth remains elusive. Herein, we investigated whether the mTOR pathway is implicated in insulin-induced mammary tumor progression in a transgenic mouse model of type 2 diabetes (MKR mice) and evaluated the impact of mTOR inhibition on the diabetic state. Mammary tumor progression was studied in the double transgenic MMTV-Polyoma Virus middle T antigen (PyVmT)/MKR mice and by orthotopic inoculation of PyVmT- and Neu/ErbB2-driven mammary tumor cells (Met-1 and MCNeuA cells respectively). mTOR inhibition by rapamycin markedly suppressed tumor growth in both wild-type and MKR mice. In diabetic animals, however, the promoting action of insulin on tumor growth was completely blunted by rapamycin, despite a worsening of the carbohydrate and lipid metabolism. Taken together, pharmacological mTOR blockade is sufficient to abrogate mammary tumor progression in the setting of hyperinsulinemia, and thus mTOR inhibitors may be an attractive therapeutic modality for breast cancer patients with type 2 diabetes. Careful monitoring of the metabolic state, however, is important as dose adaptations of glucose- and/or lipid-lowering therapy might be necessary.

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