PFKFB4 promotes lung adenocarcinoma progression via phosphorylating and activating transcriptional coactivator SRC-2
| Autor: | Xuxin Chen, Zhihai Han, Jiguang Meng |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
Pulmonary and Respiratory Medicine
Transcriptional Activation Lung Neoplasms CARM1 Phosphofructokinase-2 Adenocarcinoma of Lung Lung adenocarcinoma (LUAD) 03 medical and health sciences Nuclear Receptor Coactivator 2 0302 clinical medicine Western blot PFKFB4 Cell Movement Cell Line Tumor medicine Humans Neoplasm Invasiveness Phosphorylation Receptor 030304 developmental biology Cell Proliferation lcsh:RC705-779 0303 health sciences Gene knockdown medicine.diagnostic_test business.industry Gene Expression Profiling SRC-2 lcsh:Diseases of the respiratory system medicine.disease Gene Expression Regulation Neoplastic HEK293 Cells A549 Cells 030220 oncology & carcinogenesis Cancer research Disease Progression Adenocarcinoma business Proto-oncogene tyrosine-protein kinase Src Research Article |
| Zdroj: | BMC Pulmonary Medicine BMC Pulmonary Medicine, Vol 21, Iss 1, Pp 1-13 (2021) |
| ISSN: | 1471-2466 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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