Exploring the Effect of Differentially Expressed Long Non-coding RNAs Driven by Copy Number Variation on Competing Endogenous RNA Network by Mining Lung Adenocarcinoma Data

Abstract

Lung cancer is the first cause of cancer death, and gene copy number variation (CNV) is a vital cause of lung cancer progression. Prognosis prediction of patients followed by medication guidance by detecting CNV of lung cancer is emerging as a promising precise treatment in the future. In this paper, the differences in CNV and gene expression between cancer tissue and normal tissue of lung adenocarcinoma (LUAD) from The Cancer Genome Atlas Lung Adenocarcinoma data set were firstly analyzed, and greater differences were observed. Furthermore, CNV-driven differentially expressed long non-coding RNAs (lncRNAs) were screened out, and then, a competing endogenous RNA (ceRNA) regulatory network related to the gene CNV was established, which involved 9 lncRNAs, seven microRNAs, and 178 downstream messenger RNAs (mRNAs). Pathway enrichment analyses sequentially performed revealed that the downstream mRNAs were mainly enriched in biological pathways related to cell division, DNA repair, and so on, indicating that these mRNAs mainly affected the replication and growth of tumor cells. Besides, the relationship between lncRNAs and drug effects was explored based on previous studies, and it was found that LINC00511 and LINC00942 in the CNV-associated ceRNA network could be used to determine tumor response to drug treatment. As examined, the drugs affected by these two lncRNAs mainly targeted metabolism, target of rapamycin signaling pathway, phosphatidylinositol-3-kinase signaling pathway, epidermal growth factor receptor signaling pathway, and cell cycle. In summary, the present research was devoted to analyzing CNV, lncRNA, mRNA, and microRNA of lung cancer, and nine lncRNAs that could affect the CNV-associated ceRNA network we constructed were identified, two of which are promising in determining tumor response to drug treatment.

RETRACTED ARTICLE: LncRNA LINC00520 aggravates cell proliferation and migration in lung adenocarcinoma via a positive feedback loop

“…Many lncRNAs including ITGB1-DT [ 10 ], LINC01426 [ 11 ], UPLA1 [ 12 ] have been revealed to promote LUAD cell migration and invasion. Mechanistically, the competing endogenous RNA (ceRNA) pattern has been widely reported to be involved in LUAD progression [ 13 – 15 ]. The ceRNA network refers to that lncRNAs bind with microRNAs (miRNAs) to suppress the degradation of the targets of the miRNAs [ 16 ].…”

Immune-Related lncRNA Pairs as Prognostic Signature and Immune-Landscape Predictor in Lung Adenocarcinoma

“…AC022784.1 (12), TDRKH-AS1 (29), and LINC00941 (29) had been reported to be associated with the prognosis of LUAD. LINC00942, LINC01116, SNHG4, MIR31HG, and LINC00460 had been known to be associated with tumor development and progression and drug resistance in various cancers including lung cancer (30)(31)(32)(33)(34)(35)(36)(37)(38)(39). AC107959.3 (40) and LINC02154 (41) were reported to be associated with the prognosis of hepatocellular carcinoma and laryngeal cancer respectively.…”

Risk Scores Based on Six Survival-Related RNAs in a Competing Endogenous Network Composed of Differentially Expressed RNAs Between Clear Cell Renal Cell Carcinoma Patients Carrying Wild-Type or Mutant Von Hippel–Lindau Serve Well to Predict Malignancy and Prognosis

“…Similarly, LINC00942 was identified as one of four immune-related lncRNAs to predict prognosis and immunotherapy efficiency in bladder cancer patients ( 31 ). It also reported that LINC00942 was identified as one of the two components in a ceRNA network associated with gene number copy variation, which can be used to predict tumor response to drug treatment in patients with lung adenocarcinomas ( 32 ). Initially, LINC00858 was identified as a ceRNA impacting miR-422a to control the expression of kallikrein-related peptidase 4, and its high expression was found to be closely correlated to tumor progression of non-small cell lung carcinomas ( 33 ).…”