Abstract
Chordin-like 1 (CHRDL1), an inhibitor of bone morphogenetic proteins(BMPs), has been recently reported to participate in the progression of numerous tumors, however, its role in lung adenocarcinoma (LUAD) remains unclear. Our study aimed to demonstrate relationship between CHRDL1 and LUAD based on data from The Cancer Genome Atlas (TCGA). Among them, CHRDL1 expression revealed promising power for distinguishing LUAD tissues form normal sample. Low CHRDL1 was correlated with poor clinicopathologic features, including high T stage (OR=0.45, P<0.001), high N stage (OR=0.57, P<0.003), bad treatment effect (OR=0.64, P=0.047), positive tumor status (OR=0.63, P=0.018), and TP53 mutation (OR=0.49, P<0.001). The survival curve illustrated that low CHRDL1 was significantly correlative with a poor overall survival (HR=0.60, P<0.001). At multivariate Cox regression analysis, CHRDL1 remained independently correlative with overall survival. GSEA identified that the CHRDL1 expression was related to cell cycle and immunoregulation. Immune infiltration analysis suggested that CHRDL1 was significantly correlative with 7 kinds of immune cells. Immunohistochemical validation showed that CHRDL1 was abnormally elevated and negatively correlated with Th2 cells in LUAD tissues. In conclusion, CHRDL1 might become a novel prognostic biomarker and therapy target in LUAD. Moreover, CHRDL1 may improve the effectiveness of immunotherapy by regulating immune infiltration.
Highlights
Lung cancer remains the malignant tumor with the highest mortality around the world and has seriously burdened our health and economics for a long time [1, 2]
The expression of Chordin-like 1 (CHRDL1) was visualized in normal samples and lung adenocarcinoma (LUAD) samples based on GTEx and The Cancer Genome Atlas (TCGA)
CHRDL1 expression of tumor tissues was significantly decreased compared with normal samples in LUAD (Figure1A, P
Summary
Lung cancer remains the malignant tumor with the highest mortality around the world and has seriously burdened our health and economics for a long time [1, 2]. Lung adenocarcinoma (LUAD) is the most common subtype of NSCLC [3]. Patients with early LUAD do not have specific symptoms, so they often progress to advanced patients at the time of diagnosis. In the past ten years, targeted therapy has made significant progress in lung cancer [5]. Several genes have been applied as drug targets, such as epidermal growth factor receptor (EGFR), anaplastic lymphoma kinase (ALK), ROS1, RET, HER2, Kras and MET [6,7,8]. Drugs explored based on these genes have shown exciting efficacy [9]. It is vital to continually identify more efficient prognostic biomarkers and other potential therapy targets [11]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
