脊索蛋白样1(CHRDL1),骨形态发生蛋白(BMPs)的抑制剂,最近有报道称参与了许多肿瘤的进展,然而,其在肺腺癌(LUAD)中的作用尚不清楚。我们的研究旨在根据癌症基因组图谱(TCGA)的数据证明CHRDL1和LUAD之间的关系。其中,CHRDL1表达揭示了从正常样本中区分LUAD组织的有希望的能力。低CHRDL1与不良的临床病理特征相关,包括高T阶段(OR=0.45,P<0.001),高氮阶段(OR=0.57,P<0.003),治疗效果差(OR=0.64,P=0.047),阳性肿瘤状态(OR=0.63,P=0.018),TP53突变(OR=0.49,P<0.001)。生存曲线显示低CHRDL1与低总生存显著相关(HR=0.60,P<0.001)。在多变量Cox回归分析中,CHRDL1与总生存期保持独立相关。GSEA鉴定CHRDL1的表达与细胞周期和免疫调节有关。免疫浸润分析表明CHRDL1与7种免疫细胞显著相关。免疫组织化学验证显示CHRDL1在LUAD组织中异常升高且与Th2细胞呈负相关。总之,CHRDL1可能成为LUAD的一个新的预后生物标志物和治疗靶点。此外,CHRDL1可能通过调节免疫浸润来提高免疫治疗的有效性。
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.