scholarly journals Chromosome 17p Deletion in Human Medulloblastoma: A Missing Checkpoint in the Hedgehog Pathway

Cell Cycle ◽  
2004 ◽  
Vol 3 (10) ◽  
pp. 1263-1266 ◽  
Author(s):  
Enrico De Smaele ◽  
Lucia Di Marcotullio ◽  
Elisabetta Ferretti ◽  
Isabella Screpanti ◽  
Edoardo Alesse ◽  
...  
2019 ◽  
Vol 1 (1) ◽  
Author(s):  
Javier de la Rosa ◽  
Mónica Sánchez ◽  
Mónica Enguita-Germán ◽  
Ricardo García-López ◽  
Paula Schiapparelli ◽  
...  

2006 ◽  
Vol 175 (4S) ◽  
pp. 143-143
Author(s):  
Aubie Shaw ◽  
Jerry Gipp ◽  
Wade Bushman

2021 ◽  
Vol 12 (2) ◽  
Author(s):  
Xiaoli Liu ◽  
Zuwei Yin ◽  
Linping Xu ◽  
Huaimin Liu ◽  
Lifeng Jiang ◽  
...  

AbstractLong noncoding RNAs (lncRNAs) play crucial roles in regulating a variety of biological processes in lung adenocarcinoma (LUAD). In our study, we mainly explored the functional roles of a novel lncRNA long intergenic non-protein coding RNA 1426 (LINC01426) in LUAD. We applied bioinformatics analysis to find the expression of LINC01426 was upregulated in LUAD tissue. Functionally, silencing of LINC01426 obviously suppressed the proliferation, migration, epithelial–mesenchymal transition (EMT), and stemness of LUAD cells. Then, we observed that LINC01426 functioned through the hedgehog pathway in LUAD. The effect of LINC01426 knockdown could be fully reversed by adding hedgehog pathway activator SAG. In addition, we proved that LINC01426 could not affect SHH transcription and its mRNA level. Pull-down sliver staining and RIP assay revealed that LINC01426 could interact with USP22. Ubiquitination assays manifested that LINC01426 and USP22 modulated SHH ubiquitination levels. Rescue assays verified that SHH overexpression rescued the cell growth, migration, and stemness suppressed by LINC01426 silencing. In conclusion, LINC01426 promotes LUAD progression by recruiting USP22 to stabilize SHH protein and thus activate the hedgehog pathway.


2021 ◽  
Vol 30 ◽  
pp. 096368972098511
Author(s):  
Gang Li ◽  
Xu Zhang ◽  
Xiangyang Guo ◽  
Yi Li ◽  
Chong Li

Bladder cancer is one of the most common malignancies. The existence of bladder cancer stem cells (BCSCs) has been suggested to underlie bladder tumor initiation and recurrence. Propofol is a commonly used intravenous anesthetic. Here, we find that propofol can dramatically block the activation of Hedgehog pathway in BCSCs. The propofol strongly repressed the growth of cancer cells. Attenuated proliferation and enhanced apoptosis of tumor cells were observed upon propofol stimulation. Furthermore, propofol reduced the self-renewal ability of BCSCs as well as the tumor formation. In conclusion, propofol is potentially used as a novel therapeutic agent for bladder cancer by targeting self-renewal through inhibiting Hedgehog pathway.


2009 ◽  
Vol 361 (12) ◽  
pp. 1173-1178 ◽  
Author(s):  
Charles M. Rudin ◽  
Christine L. Hann ◽  
John Laterra ◽  
Robert L. Yauch ◽  
Christopher A. Callahan ◽  
...  

2009 ◽  
Vol 361 (12) ◽  
pp. 1164-1172 ◽  
Author(s):  
Daniel D. Von Hoff ◽  
Patricia M. LoRusso ◽  
Charles M. Rudin ◽  
Josina C. Reddy ◽  
Robert L. Yauch ◽  
...  

2012 ◽  
Vol 3 (10) ◽  
pp. 808-813 ◽  
Author(s):  
Chris Dockendorff ◽  
Marek M. Nagiec ◽  
Michel Weïwer ◽  
Sara Buhrlage ◽  
Amal Ting ◽  
...  

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