scholarly journals Molecular Cloning and Functional Characterization of a Cell-permeable Superoxide Dismutase Targeted to Lung Adenocarcinoma Cells

2006 ◽  
Vol 281 (19) ◽  
pp. 13620-13627 ◽  
Author(s):  
Min Lu ◽  
Xingguo Gong ◽  
Yuwen Lu ◽  
Jianjun Guo ◽  
Chenhui Wang ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Lung Adenocarcinoma ◽  
Molecular Cloning ◽  
Functional Characterization ◽  
Adenocarcinoma Cells ◽  
A Cell ◽  
Lung Adenocarcinoma Cells

scholarly journals Generation of Stable cisPt Resistant Lung Adenocarcinoma Cells

2020 ◽  
Vol 13 (6) ◽  
pp. 109 ◽  
Author(s):  
Nico Ruprecht ◽  
Lukas Hofmann ◽  
Martin Nils Hungerbühler ◽  
Christoph Kempf ◽  
Johannes Thomas Heverhagen ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Lung Adenocarcinoma ◽  
Acquired Resistance ◽  
Advanced Lung Cancer ◽  
Anion Channels ◽  
Mechanisms Of Resistance ◽  
Adenocarcinoma Cells ◽  
A Cell ◽  
Lung Adenocarcinoma Cells ◽  
High Level

Platinum compounds represent the backbone of combined chemotherapy protocols for advanced lung cancer. The mechanisms responsible for its frequent primary or acquired resistance to cisplatin (cisPt)-based chemotherapy remains enigmatic. The availability of two cell lines of the same origin, one resistant and the other sensitive, will facilitate research to reveal the mechanism of resistance formation. Lung adenocarcinoma cells, A240286S (A24), were cultivated in increasing cisPt concentrations over a prolonged time. After a significant increase in IC50 was measured, cultivation of the cells was continued in absence of cisPt and IC50s determined over a long period (>7 months). As a result, a cell line with lasting, high-level cisPt resistance, designated (D-)A24cisPt8.0, was obtained. The cells were cross-resistant to oxaliplatin and to pemetrexed at a low level. Previous publications have claimed that Leucine-rich repeat-containing protein 8 (LRRC8A and LRRC8D) of the volume-regulated anion channels (VRACs) affect cellular resistance to cisPt. Even though cisPt decreased LRRC8D expression levels, we showed by knockdown and overexpression experiments with LRRC8A and D that these proteins do not govern the observed cisPt resistance. The tumor cell sublines described here provide a powerful model to study the mechanisms of resistance to cisPt in lung cancer cells and beyond.

scholarly journals PFKFB4 promotes lung adenocarcinoma progression via phosphorylating and activating transcriptional coactivator SRC-2

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Jiguang Meng ◽  
Xuxin Chen ◽  
Zhihai Han
Keyword(s):  
Lung Adenocarcinoma ◽  
Transcriptional Activity ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Transcriptional Coactivator ◽  
Downstream Target ◽  
Steroid Receptor Coactivator ◽  
Adenocarcinoma Cells ◽  
Family Protein ◽  
Lung Adenocarcinoma Cells

Abstract Background To investigate the role and its potential mechanism of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 4 (PFKFB4) in lung adenocarcinoma. Methods Co-immunoprecipitation was performed to analyze the interaction between PFKFB4 and SRC-2. Western blot was used to investigate the phosphorylation of steroid receptor coactivator-2 (SRC-2) on the condition that PFKFB4 was knockdown. Transcriptome sequencing was performed to find the downstream target of SRC-2. Cell Counting Kit-8 (CCK-8) assay, transwell assay and transwell-matrigel assay were used to examine the proliferation, migration and invasion abilities in A549 and NCI-H1975 cells with different treatment. Results In our study we found that PFKFB4 was overexpressed in lung adenocarcinoma associated with SRC family protein and had an interaction with SRC-2. PFKFB4 could phosphorylate SRC-2 at Ser487, which altered SRC-2 transcriptional activity. Functionally, PFKFB4 promoted lung adenocarcinoma cells proliferation, migration and invasion by phosphorylating SRC-2. Furthermore, we identified that CARM1 was transcriptionally regulated by SRC-2 and involved in PFKFB4-SRC-2 axis on lung adenocarcinoma progression. Conclusions Our research reveal that PFKFB4 promotes lung adenocarcinoma cells proliferation, migration and invasion via enhancing phosphorylated SRC-2-mediated CARM1 expression.

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