Tacrolimus and ascomycin inhibit melanoma cell growth, migration and invasion via targeting nuclear factor of activated T-cell 3

2020 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Tian Xiao ◽  
Wencong Chen ◽  
Shuangfeng Wang ◽  
Shiying Huang ◽  
Chengyao Chiang ◽  
...  
2018 ◽  
Vol 131 (3) ◽  
pp. 330-338 ◽  
Author(s):  
Xiu-Ping Xu ◽  
Yong-Ming Yao ◽  
Guang-Ju Zhao ◽  
Zong-Sheng Wu ◽  
Jun-Cong Li ◽  
...  

2019 ◽  
Vol 52 (4) ◽  
pp. 172
Author(s):  
Nirawati Pribadi ◽  
Rosita Rahmawati ◽  
Mandojo Rukmo ◽  
Adelina Kristanti Tandadjaja ◽  
Hendy Jaya Kurniawan ◽  
...  

Background: Enterococcus faecalis (E. faecalis) is the most common bacteria species in persistent endodontic infection of teeth undergoing root canal treatment at a prevalence of 38%. The virulence factor of this bacterium is Lipoteichoic acid (LTA) which can be recognized by Toll-like receptors-4 (TLR-4) that produce a stimulus and provoke an immune response. Inflammation results in bone defects that feature multiple cytokines and interactions between different cell types. Bone loss within a periapical tooth is characterized by osteoclast formation (osteoclastogenesis) in the bone. Purpose: This study aimed to determine the expression of nuclear factor of activated T cell c1 (NFATc1) and receptor activator of nuclear factor kappa β (RANK) which played a role in osteoclastogenesis at different time intervals. Methods: 36 upper molar teeth of the research subjects were induced with 106 CFU Enterococcus faecalis and subsequently observed for 7 and 21 days with the NFATc1 and RANK being counted microscopically at 1000X magnification across 20 viewing fields. Thereafter, the data was examined and analyzed by means of an independent T test using SPSS. Results: NFATc1 and RANK expression were higher in the group including E. faecalis on days 7 and 21 than in the control group. There were significant differences between the treatment group and control group with regard to NFATc1 and RANK expression (p<0.05). Conclusion: The study showed that the expression of NFATc1 and RANK, which plays a role in osteoclastogenesis, was higher in periapical bone defects in Wistar rats induced by E. faecalis than those which were not induced.


2003 ◽  
Vol 278 (18) ◽  
pp. 15550-15557 ◽  
Author(s):  
Seung-jae Kim ◽  
Wei Ding ◽  
Björn Albrecht ◽  
Patrick L. Green ◽  
Michael D. Lairmore

2007 ◽  
Vol 1117 (1) ◽  
pp. 138-142 ◽  
Author(s):  
A. B. CELIL AYDEMIR ◽  
S. LEE ◽  
D. WON KIM ◽  
T. R. GARDNER ◽  
D. PRINCE ◽  
...  

2012 ◽  
Vol 23 (15) ◽  
pp. 2963-2972 ◽  
Author(s):  
Yuning Zhou ◽  
Qingding Wang ◽  
Zheng Guo ◽  
Heidi L. Weiss ◽  
B. Mark Evers

The nuclear factor of activated T-cell (NFAT) proteins are a family of transcription factors (NFATc1–c4) involved in the regulation of cell differentiation. We identified REDD1, a negative regulator of mammalian target of rapamycin (mTOR) through the tuberous sclerosis complex (TSC1/2 complex), as a new molecular target of NFATc3. We show that treatment with a combination of phorbol 12-myristate 13-acetate (PMA) plus ionophore A23187 (Io), which induces NFAT activation, increased REDD1 mRNA and protein expression and inhibited mTOR signaling; pretreatment with the calcineurin inhibitor cyclosporin A (CsA), an antagonist of NFAT signaling, decreased REDD1 induction and mTOR inhibition. Knockdown of NFATc3, not NFATc1, NFATc2, or NFATc4, attenuated PMA/Io-induced REDD1 expression. Treatment with PMA/Io increased REDD1 promoter activity and increased NFATc3 binding to the REDD1 promoter. Overexpression of NFATc3 increased REDD1 mRNA and protein expression and increased PMA/Io-mediated REDD1 promoter activity. Treatment with PMA/Io increased expression of the goblet cell differentiation marker MUC2; these changes were attenuated by pretreatment with CsA or knockdown of REDD1 or NFATc3. Overexpression of NFATc3 increased, while knockdown of TSC2 decreased, MUC2 expression. We provide evidence showing NFATc3 inhibits mTOR via induction of REDD1. Our results suggest a role for the NFATc3/REDD1/TSC2 axis in the regulation of intestinal cell differentiation.


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