scholarly journals TRIM55 suppresses malignant biological behavior of lung adenocarcinoma cells by increasing protein degradation of Snail1

2022 ◽  
pp. 1-10
Author(s):  
Tianxing Guo ◽  
Zhenlong Zhang ◽  
Lihuan Zhu ◽  
Wenshu Chen ◽  
Yun Ding ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Protein Degradation ◽  
Biological Behavior ◽  
Adenocarcinoma Cells ◽  
Lung Adenocarcinoma Cells

scholarly journals Influence of Autophagy Inhibition on Lung Adenocarcinoma Cell Migration and Invasion Ability, and Efficacy of Gefitinib

2021 ◽  
Vol 20 ◽  
pp. 153303382110490
Author(s):  
Ying Liu ◽  
Yun Du
Keyword(s):  
Lung Adenocarcinoma ◽  
Kinase Inhibitors ◽  
Malignant Tumors ◽  
Growth Factor Receptor ◽  
Scratch Test ◽  
Biological Behavior ◽  
Migration And Invasion ◽  
Adenocarcinoma Cells ◽  
Lung Adenocarcinoma Cells ◽  
Autophagy Inhibition

An increasing number of studies have emphasized the role of autophagy in cancer cell metastasis and treatment of malignant tumors. Autophagy inhibitors have been widely used in combination therapies to treat advanced malignancies. Several lung adenocarcinoma cells harbor epidermal growth factor receptor (EGFR) gene mutations, and EGFR tyrosine kinase inhibitors (TKIs) are routinely used in the treatment of lung adenocarcinoma. However, a number of lung adenocarcinoma tumors do not respond or develop resistance to EGFR TKIs. The aim of the present study was to explore the effect of autophagy inhibition on the biological behavior of lung adenocarcinoma cells. In addition, whether autophagy inhibition increases the efficacy of gefitinib in lung adenocarcinoma was investigated. The activation of autophagy was inhibited via the reduction of the expression of ATG5 in A549, H1975 and HCC827 cells. ATG5 knockdown using ATG5 siRNA partially suppressed the LC3B-II expression, decreased the LC3B-I/II conversion rate and enhanced the P62 expression. Cell scratch test and Transwell assay showed that the inhibition of autophagy could impair the migration and invasion ability of cells. These studies suggested that autophagy may play a pro-survival role in lung adenocarcinoma.

scholarly journals P5CR1 protein expression and the effect of gene-silencing on lung adenocarcinoma

PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e6934 ◽  
Author(s):  
Yang She ◽  
Aiyou Mao ◽  
Feng Li ◽  
Xiaobin Wei
Keyword(s):  
Protein Expression ◽  
Lung Adenocarcinoma ◽  
Gene Silencing ◽  
Therapeutic Target ◽  
Biological Behavior ◽  
Pathological Grade ◽  
Adenocarcinoma Cells ◽  
Cisplatin Sensitivity ◽  
Lung Adenocarcinoma Cells ◽  
And Gender

The present study aimed to investigate the expression of pyrroline-5-carboxylate reductase 1 (P5CR1) protein in lung adenocarcinoma and paracancerous tissues and to explore the effect of silencing the encoding gene PYCR1 on the proliferation, migration, invasion, and cisplatin sensitivity in lung adenocarcinoma cells, thereby providing a novel therapeutic target for the treatment of the disease. Immunohistochemistry staining was used to detect the P5CR1 protein expression in lung adenocarcinoma and paracancerous tissues, and statistical analysis evaluated the correlation between P5CR1 protein expression and gender, age, tissue part, or pathological grade. The CCK8 assay was performed to detect the proliferation and cisplatin sensitivity, while the effect of PYCR1 on the migration and invasion of lung adenocarcinoma cells was detected by scratch test and transwell chamber assay. The findings demonstrated that the P5CR1 protein expression was significantly elevated in lung adenocarcinoma tissues and correlated with the pathological grade, whereas no significant correlation was established between the protein expression and gender, age, or tissue part. Furthermore, after PYCR1 gene silencing, the proliferation and invasion were significantly suppressed, while the sensitivity to cisplatin was significantly enhanced. Therefore, it can be speculated that the PYCR1 gene affects the biological behavior of lung adenocarcinoma and cisplatin resistance, serving as a potential therapeutic target for lung adenocarcinoma.

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.

scholarly journals PD-L1 lncRNA splice isoform promotes lung adenocarcinoma progression via enhancing c-Myc activity

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Shuang Qu ◽  
Zichen Jiao ◽  
Geng Lu ◽  
Bing Yao ◽  
Ting Wang ◽  
...  
Keyword(s):  
Alternative Splicing ◽  
Lung Adenocarcinoma ◽  
Solid Tumors ◽  
Immune Checkpoint ◽  
Checkpoint Inhibition ◽  
Immune Checkpoint Inhibition ◽  
Non Coding Rna ◽  
Adenocarcinoma Cells ◽  
Lung Adenocarcinoma Cells ◽  
Long Non Coding Rna

Abstract Background Although using a blockade of programmed death-ligand 1 (PD-L1) to enhance T cell immune responses shows great promise in tumor immunotherapy, the immune-checkpoint inhibition strategy is limited for patients with solid tumors. The mechanism and efficacy of such immune-checkpoint inhibition strategies in solid tumors remains unclear. Results Employing qRT-PCR, Sanger sequencing, and RNA BaseScope analysis, we show that human lung adenocarcinoma (LUAD) all produce a long non-coding RNA isoform of PD-L1 (PD-L1-lnc) by alternative splicing, regardless if the tumor is positive or negative for the protein PD-L1. Similar to PD-L1 mRNA, PD-L1-lnc in various lung adenocarcinoma cells is significantly upregulated by IFNγ. 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 promotes lung adenocarcinoma progression through directly binding to c-Myc and enhancing c-Myc transcriptional activity. Conclusions In summary, the PD-L1 gene can generate a long non-coding RNA through alternative splicing to promote lung adenocarcinoma progression by enhancing c-Myc activity. Our results argue in favor of investigating PD-L1-lnc depletion in combination with PD-L1 blockade in lung cancer therapy.

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