ABSTRACT
Exosomes are tiny vesicles produced in cells which sizes between 40 to 100 nm. Exosomes are carriers of cell signal transduction. Thyroid cancer is the common malignant tumor in endocrine system. Exosomes show the regulatory role in thyroid cancer about occurrence, development and metastasis. This review focuses on the relevant characteristics of exosomes and the research progress of exosomes in thyroid cancer.
ABSTRACT
Exosomes are tiny vesicles produced in cells which sizes between 40 to 100 nm.Exosomes are carriers of cell signal transduction.Thyroid cancer is the common malignant tumor in endocrine system.Exosomes show the regulatory role in thyroid cancer about occurrence,development and metastasis.This review focuses on the relevant characteristics of exosomes and the research progress of exosomes in thyroid cancer.
ABSTRACT
Objective To investigate the effects of Arctigenin ( ATG ) on concanavalin ( ConA )-stimulated cell proliferation and cytokine secretion in mouse spleen cells, and its possible mechanism. Methods The toxicity of ATG on mouse spleen cells was determined by MTT assay. The inhibition of proliferation was investigated by tritiat-ed thymidine incorporation method. Secreted cytokines (IFN-γand IL-2) were analyzed by ELISA. The associated proteins and phosphorylation levels of mTOR pathway ( mTOR/P70 S6 K/Akt/AMPK/Raptor ) were detected by Western blot. Results ATG had no significant toxicity to mouse spleen cells. ATG significantly inhibited mouse primary spleen cells proliferation induced by ConA. ATG suppressed IL-2 and IFN-γ production of mouse spleen cells in a concentration-dependent manner. ATG remarkably suppressed the phosphorylation of mTOR and P70S6K, and enhanced the phosphorylation of upstream AMPK and Raptor, while the phosphorylation of Akt did not change significantly. Conclusion ATG markedly suppresses the proliferation of mouse spleen stimulated by ConA cells and secretion of IFN-γand IL-2 , which may be correlated to the abilities of enhancing the phosphoryla-tion of AMPK and Raptor, inhibiting the phosphorylation of mTOR and P70S6K.