Abstract
BackgroundThe crucial roles played by lncRNA-AC068228.1 in primary malignant cancer remain poorly understood. This study aimed at examining the clinical significance and evaluating the biological function of AC068228.1 in lung adenocarcinoma (LUAD).MethodsWe used data obtained from The Cancer Genome Atlas (TCGA), Genotype-Tissue Expression (GTEx), and the Gene Expression Omnibus (GEO) database to examine the expression of AC068228.1 in LUAD patients, and the prognostic and diagnostic value of those levels. Functional experiments were conducted to determine the function of AC068228.1 on LUAD cells. Signaling pathway enrichment analysis of AC068228.1 was conducted using the clusterProfiler and Gene Set Enrichment Analysis (GSEA) software. We analyzed the correlation between AC068228.1 expression and immune infiltration level in LUAD using the single-sample gene set enrichment analysis (ssGSEA) method by the R package GSVA.ResultsAC068228.1 expression was significantly elevated in LUAD tissues compared with normal tissues. Higher expression of AC068228.1 was strongly correlated with adverse clinical outcomes and was identified as an independent prognostic marker for LUAD patients. GSEA and infiltration analysis confirmed that AC068228.1 expression was significantly correlated with immune cells infiltrating in LUAD. Knockdown of AC068228.1 inhibited the cell proliferation and cell migration of LUAD.ConclusionsAC068228.1 was upregulated in LUAD and was significantly correlated with adverse clinical outcomes. Meanwhile, it was associated with immune cell infiltration and could be used as a promising diagnostic and prognostic biomarker for LUAD patients.
Highlights
Lung cancer is the leading cause of cancer-related morbidity and mortality worldwide [1]
Results showed that AC068228.1 was highly expressed in 15 tumor types, including adrenocortical carcinoma (ACC), bladder urothelial carcinoma (BLCA), breast invasive carcinoma (BRCA), cervical squamous cell carcinoma and endocervical adenocarcinoma (CESC), colon adenocarcinoma (COAD), head and neck squamous cell carcinoma (HNSC), lung adenocarcinoma (LUAD), lung squamous cell carcinoma (LUSC), ovarian serous cystadenocarcinoma (OV), pancreatic adenocarcinoma (PAAD), rectum adenocarcinoma (READ), stomach adenocarcinoma (STAD), thyroid carcinoma (THCA), thymoma (THYM), and uterine corpus endometrial carcinoma (UCEC) (Figure 1A)
AC068228.1 was upregulated in LUAD in GSE81089 datasets, which is consistent with the The Cancer Genome Atlas (TCGA) database we discovered (Figure 1C)
Summary
Lung cancer is the leading cause of cancer-related morbidity and mortality worldwide [1]. Expressed lncRNAs have been reported to correlate with the development and progression of lung cancer [9]. Gong et al found that lncRNA JPX was highly expressed in lung cancer and correlated with the tumor size and an advanced stage. Forced expression of JPX facilitated lung cancer cell proliferation in vitro and facilitated lung tumor growth in vivo [10]. Further research showed that lnc-IGFBP4-1 via affecting the expression of HK2, PDK1, and LDHA led to enhancement of the ATP production level and involvement in lung cancer progression [11]. LncRNA AFAP1-AS1 was found to modulate NSCLC cell proliferation via interacting with EZH2 and recruiting EZH2 to the promoter regions of p21, inhibiting p21 expression [12]. This study aimed at examining the clinical significance and evaluating the biological function of AC068228.1 in lung adenocarcinoma (LUAD)
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