W1953 Effect of a Novel Telomerase Inhibitor, Grn163l, On Growth of Barrett's Esophageal Adenocarcinoma Cells In Vitro and In Vivo

2008 ◽  
Vol 134 (4) ◽  
pp. A-741
Author(s):  
Masood A. Shammas ◽  
Aamer Qazi ◽  
Ramesh B. Batchu ◽  
Robert C. Bertheau ◽  
Jason Y. Wong ◽  
...  
2010 ◽  
Vol 28 (4) ◽  
pp. 1089-1100 ◽  
Author(s):  
Kejun Zhang ◽  
Shaoyan Zhang ◽  
Xuelong Jiao ◽  
Haibo Wang ◽  
Dianliang Zhang ◽  
...  

2016 ◽  
Vol 61 (10) ◽  
pp. 2896-2907 ◽  
Author(s):  
Elena Piazuelo ◽  
Paula Esquivias ◽  
Alba De Martino ◽  
Carmelo Cebrián ◽  
Blanca Conde ◽  
...  

2008 ◽  
Vol 134 (4) ◽  
pp. A-741
Author(s):  
Masood A. Shammas ◽  
Christopher S. Bryant ◽  
Sanjeev Kumar ◽  
Madhu Prasad ◽  
Christopher P. Steffes ◽  
...  

2020 ◽  
Author(s):  
Shuang Qu ◽  
Zichen Jiao ◽  
Geng Lu ◽  
Bing Yao ◽  
Ting Wang ◽  
...  

ABSTRACTAlthough blockade of programmed death-ligand 1 (PD-L1) to enhance T cell immune responses shows great promise in tumor immunotherapy, the efficacy of such immune-checkpoint inhibition strategy is limited for patients with solid tumors. The mechanism underlying the limited efficacy of PD-L1 inhibitors remains unclear. Here, we show that human lung adenocarcinoma, regardless of PD-L1 protein positive or negative, all produce a long non-coding RNA isoform of PD-L1 (PD-L1-lnc) via alternative splicing, which promotes lung adenocarcinoma proliferation and metastasis. PD-L1-lnc in various lung adenocarcinoma cells is significantly upregulated by IFNγ in a manner similar to PD-L1 mRNA. Both in vitro and in vivo studies demonstrate that PD-L1-lnc increases proliferation and invasion but decreases apoptosis of lung adenocarcinoma cells. Mechanistically, PD-L1-lnc directly binds to c-Myc and enhances c-Myc transcriptional activity downstream in lung adenocarcinoma cells. Our results provide targeting PD-L1-lnc−c-Myc axis as a novel strategy for lung cancer therapy.


2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Fu-Tao Chen ◽  
Fu-Kuan Zhong

Objective. To determine the expression levels of KIF18A in lung adenocarcinoma and its relationship with the clinicopathologic features of patients undergoing radical colectomy and explore the potential role in the progression of lung adenocarcinoma. Methods. Immunohistochemical assays were performed to explore the expression levels of KIF18A in 82 samples of lung adenocarcinoma and corresponding normal tissues. According to the levels of KIF18A expression in lung adenocarcinoma tissue samples, patients were classified into the KIF18A high expression group and low expression group. Clinical data related to the perioperative clinical features (age, gender, smoking, tumor size, differentiation, clinical stage, and lymph node metastasis), the potential correlation between KIF18A expression levels, and clinical features were analyzed, and the effects of KIF18A on lung adenocarcinoma cell proliferation, migration, and invasion were measured by colony formation assay, MTT assay, wound healing assay, and transwell assays. The possible effects of KIF18A on tumor growth and metastasis were measured in mice through tumor growth and tumor metastasis assays in vivo. Results. KIF18A in lung adenocarcinoma tissues. Further, KIF18A was significantly associated to clinical characteristic features including the tumor size (P=0.033) and clinical stage (P=0.041) of patients with lung adenocarcinoma. Our data also investigated that KIF18A depletion dramatically impairs the proliferation, migration, and invasion capacity of lung adenocarcinoma cells in vitro and inhibits tumor growth and metastasis in mice. Conclusions. Our study reveals the involvement of KIF18A in the progression and metastasis of lung adenocarcinoma and provides a novel therapeutic target for the treatment of lung adenocarcinoma.


2018 ◽  
Author(s):  
Mylan Blomquist ◽  
Vashti M. Carson ◽  
Ross M. Bremner ◽  
Timothy G. Whitsett ◽  
Landon J. Inge

2008 ◽  
Vol 134 (4) ◽  
pp. A-441 ◽  
Author(s):  
Jin Si ◽  
Jie Hong ◽  
Jose Behar ◽  
Jack R. Wands ◽  
Rhonda F. Souza ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document