scholarly journals In vitro embryotoxicity and mode of antibacterial mechanistic study of gold and copper nanoparticles synthesized from Angelica keiskei (Miq.) Koidz. leaves extract

Author(s):  
Chandran Krishnaraj ◽  
Glenn M Young ◽  
Soon-Il Yun
2021 ◽  
Vol 143 ◽  
pp. 105564
Author(s):  
Luisa F. Cruz ◽  
Juan C. Cruz ◽  
Daniel Carrillo ◽  
Arturo I. Mtz-Enriquez ◽  
Araceli Lamelas ◽  
...  

Oncogenesis ◽  
2021 ◽  
Vol 10 (5) ◽  
Author(s):  
Dawei Zhu ◽  
Xing Gu ◽  
Zhengyu Lin ◽  
Dandan Yu ◽  
Jing Wang

AbstractGallbladder cancer (GBC) is a common malignant tumor of the biliary tract, which accounts for 80–95% of biliary tumors worldwide, and is the leading cause of biliary malignant tumor-related death. This study identified PSMC2 as a potential regulator in the development of GBC. We showed that PSMC2 expression in GBC tissues is significantly higher than that in normal tissues, while high PSMC2 expression was correlated with more advanced tumor grade and poorer prognosis. The knockdown of PSMC2 in GBC cells induced significant inhibition of cell proliferation, colony formation and cell motility, while the promotion of cell apoptosis. The construction and observation of the mice xenograft model also confirmed the inhibitory effects of PSMC2 knockdown on GBC development. Moreover, our mechanistic study recognized GNG4 as a potential downstream target of PSMC2, knockdown of which could aggravate the tumor suppression induced by PSMC2 knockdown in vitro and in vivo. In conclusion, for the first time, PSMC2 was revealed as a tumor promotor in the development of GBC, which could regulate cell phenotypes of GBC cells through the interaction with GNG4, and maybe a promising therapeutic target in GBC treatment.


2004 ◽  
Vol 62 (1) ◽  
pp. 1-11 ◽  
Author(s):  
Isabelle Ragueneau-Majlessi ◽  
Rene H. Levy ◽  
Donna Bergen ◽  
William Garnett ◽  
William Rosenfeld ◽  
...  

2015 ◽  
Vol 38 ◽  
pp. e20-e21
Author(s):  
Thomas Minchington ◽  
Brian Tighe

2018 ◽  
Vol 81 (9) ◽  
pp. 1956-1961 ◽  
Author(s):  
Nikhil B. Ghate ◽  
Dipankar Chaudhuri ◽  
Sourav Panja ◽  
Sudhir S. Singh ◽  
Gajendra Gupta ◽  
...  

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Jose A. Villa-Rodriguez ◽  
Asimina Kerimi ◽  
Laszlo Abranko ◽  
Sarka Tumova ◽  
Lauren Ford ◽  
...  

2020 ◽  
Vol 117 (9) ◽  
pp. 4770-4780 ◽  
Author(s):  
Hao Jiang ◽  
Hui-Jun Cao ◽  
Ning Ma ◽  
Wen-Dai Bao ◽  
Jing-Jing Wang ◽  
...  

Recurrence and metastasis remain the major obstacles to successful treatment of hepatocellular carcinoma (HCC). Chromatin remodeling factor ARID2 is commonly mutated in HCC, indicating its important role in cancer development. However, its role in HCC metastasis is largely elusive. In this study, we find that ARID2 expression is significantly decreased in metastatic HCC tissues, showing negative correlation with pathological grade, organ metastasis and positive association with survival of HCC patients. ARID2 inhibits migration and invasion of HCC cells in vitro and metastasis in vivo. Moreover, ARID2 knockout promotes pulmonary metastasis in different HCC mouse models. Mechanistic study reveals that ARID2 represses epithelial–mesenchymal transition (EMT) of HCC cells by recruiting DNMT1 to Snail promoter, which increases promoter methylation and inhibits Snail transcription. In addition, we discover that ARID2 mutants with disrupted C2H2 domain lose the metastasis suppressor function, exhibiting a positive association with HCC metastasis and poor prognosis. In conclusion, our study reveals the metastasis suppressor role as well as the underlying mechanism of ARID2 in HCC and provides a potential therapeutic target for ARID2-deficient HCC.


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