scholarly journals Cell line and drug-dependent effect of ERBB3 on cancer cell proliferation, chemosensitivity, and multidrug actions

Author(s):  
Jin-Xiong She
2019 ◽  
Vol 18 ◽  
pp. 153303381986197 ◽  
Author(s):  
Xiaohong Yan ◽  
Hui Yu ◽  
Yao Liu ◽  
Jie Hou ◽  
Qiao Yang ◽  
...  

MicroRNA-27a-3p has been implicated to play crucial roles in human cancers. However, the biological role and underlying mechanisms of microRNA-27a-3p in regulating nonsmall lung cancer remain unclear. MicroRNA-27a-3p expression levels in non-small lung cancer cell lines were detected by quantitative real-time polymerase chain reaction, using a normal cell line as control. The effects of microRNA-27a-3p on cell proliferation and apoptosis were analyzed by Cell Counting Kit-8 assay and flow cytometry assay. Luciferase activity reporter assay and Western blot were conducted to validate the potential targets of miR27a-3p after preliminary screening by TargetScan. Effect of microRNA-27a-3p or homeobox B8 on the overall survival of patients with non-small lung cancer was analyzed at Kaplan-Meier Plotter website. MicroRNA-27a-3p expression levels were significantly reduced in non-small lung cancer cell lines compared with normal cell line. Overexpression of microRNA-27a-3p inhibits non-small lung cancer cell proliferation but promotes cell apoptosis. Homeobox B8 was further validated as a functional target of microRNA-27a-3p. Collectively, our results indicated that microRNA-27a-3p acts as a tumor suppressor in non-small lung cancer via targeting homeobox B8.


2020 ◽  
Vol 21 (10) ◽  
pp. 3586 ◽  
Author(s):  
Yoo-Duk Choi ◽  
Ji-Yeon Jung ◽  
Minwoo Baek ◽  
Sheema Khan ◽  
Peter I. Song ◽  
...  

Pancreatic cancer is the worst exocrine gastrointestinal cancer leading to the highest mortality. Recent studies reported that aberrant expression of apurinic/apyrimidinic endodeoxyribonuclease 1 (APE1) is involved in uncontrolled cell growth. However, the molecular mechanism of APE1 biological role remains unrevealed in pancreatic cancer progression. Here, we demonstrate that APE1 accelerates pancreatic cancer cell proliferation through glial cell line-derived neurotrophic factor (GDNF)/glial factor receptor α1 (GFRα1)/Src/ERK axis-cascade signaling. The proliferation of endogenous APE1 expressed-MIA PaCa-2, a human pancreatic carcinoma cell line, was increased by treatment with GDNF, a ligand of GFRα1. Either of downregulated APE1 or GFRα1 expression using small interference RNA (siRNA) inhibited GDNF-induced cancer cell proliferation. The MEK-1 inhibitor PD98059 decreased GDNF-induced MIA PaCa-2 cell proliferation. Src inactivation by either its siRNA or Src inhibitor decreased ERK-phosphorylation in response to GDNF in MIA PaCa-2 cells. Overexpression of GFRα1 in APE1-deficient MIA PaCa-2 cells activated the phosphorylation of Src and ERK. The expression of both APE1 and GFRα1 was gradually increased as progressing pancreatic cancer grades. Our results highlight a critical role for APE1 in GDNF-induced pancreatic cancer cell proliferation through APE1/GFRα1/Src/ERK axis-cascade signaling and provide evidence for future potential therapeutic drug targets for the treatment of pancreatic cancer.


2001 ◽  
Vol 120 (5) ◽  
pp. A615-A615
Author(s):  
S KUWADA ◽  
C SCAIFE ◽  
J KUANG ◽  
R DAYNES

Planta Medica ◽  
2012 ◽  
Vol 78 (11) ◽  
Author(s):  
S Sun ◽  
M Zhang ◽  
M Li ◽  
F Guan ◽  
F Wu ◽  
...  

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1957-P
Author(s):  
TAKAKO KAWANAMI ◽  
TAKASHI NOMIYAMA ◽  
YURIKO HAMAGUCHI ◽  
TOMOKO TANAKA ◽  
TOSHIHIKO YANASE

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