Journal
BMC PULMONARY MEDICINE
Volume 21, Issue 1, Pages -Publisher
BMC
DOI: 10.1186/s12890-021-01420-x
Keywords
PFKFB4; Lung adenocarcinoma (LUAD); SRC-2; Phosphorylation
Categories
Funding
- Health Care Foundation of Logistics Support Department of Central Military Commission [17BJZ04]
- Innovative Cultivation Foundation of Sixth Medical Center of Chinese People's Liberation Army General Hospital [CXPY201729]
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PFKFB4 is overexpressed in lung adenocarcinoma and interacts with SRC-2. Phosphorylated SRC-2 by PFKFB4 promotes cancer cell proliferation, migration, and invasion. The PFKFB4-SRC-2-CARM1 axis plays a crucial role in lung adenocarcinoma progression.
BackgroundTo investigate the role and its potential mechanism of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 4 (PFKFB4) in lung adenocarcinoma.MethodsCo-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.ResultsIn 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.ConclusionsOur research reveal that PFKFB4 promotes lung adenocarcinoma cells proliferation, migration and invasion via enhancing phosphorylated SRC-2-mediated CARM1 expression.
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