Abstract 20P
Background
The morbidity and mortality of lung cancer rank the first among malignant tumors in China. EGFR-TKIs has achieved good efficacy in advanced lung adenocarcinoma with EGFR-positive, however, drug resistance and rapid progress of some patients are still inevitable. Therefore, it is of great significance to find new therapeutic targets. Abnormally activated transcriptional regulators are involved in many biological processes of the development of malignant tumors, further exploration of their functional mechanisms is expected to provide a new direction for targeted tumor therapy.
Methods
TRRUST and CHIPBase databases of transcriptional regulatory factor and TCGA databases were integrated to screen the transcriptional regulatory factors with significantly different expression in lung adenocarcinoma. The prediction of interacting molecules was performed on the Linkedomics, and preliminary verification was performed using WB. The clinicopathological data of lung adenocarcinoma patients with survival data from GEO and TCGA databases were downloaded to analyze the effect of CRABP2 and MK2 expression on survival prognosis.
Results
Transcription and protein expression of CRABP2 were significantly up-regulated in lung adenocarcinoma. Bioinformatics analysis showed that MK2 interacted with CRABP2, and CRABP2protein decreased significantly after knockdown of Mk2 protein expression. The overall survival of lung adenocarcinoma patients with high CRABP2 and MK2 expressions were worse than that of the low expression group (P = 3.4e-04 and 6.5e-05, respectively).
Conclusions
MK2 may phosphorylate CRABP2 to mediate the progression of lung adenocarcinoma, and the MK2-CRABP2 signaling pathway is expected to become a biomarker or a new target for drug therapy of lung adenocarcinoma. However, further molecular experiments are needed for further exploration and verification.
Clinical trial identification
Editorial acknowledgement
Legal entity responsible for the study
The authors.
Funding
Has not received any funding.
Disclosure
All authors have declared no conflicts of interest.