Basic Information
Regular Relationship :
Phenotype/DiseaseSpecieLung Cancer
CeRNA1RP11-89K21.1[LncRNA]
miRNAmiR-146a-5p[miRNA]
CeRNA2RHPN2[mRNA]
Tissue/Cell lineLUAD tissues and pair-matched adjacent normal tissues
SpecieHomo sapiens (human)
CitationCancer Biother Radiopharm. 2021 Apr 20. doi: 10.1089/cbr.2020.4395.
Reference title
Long Noncoding RNA RP11-89K21.1 Interacts with miR-146a/b-5p to Promote Proliferation and Gefitinib Resistance Through Regulating RHPN2 and RhoA/ROCK Pathway in Lung Adenocarcinoma.
Experimental verification
Western blot;Luciferase reporter assay;
Functional description
Background: Long noncoding RNAs (lncRNAs) have major roles in lung adenocarcinoma (LUAD). lncRNA RP11-89K21.1 was reported to be abnormally expressed in LUAD, yet its biological functions in LUAD progression remain unclear. Materials and Methods: The 40 LUAD tissues and pair-matched adjacent normal tissues were enrolled in this study. Quantitative real-time polymerase chain reaction was performed to detect the expression of lncRNA, miRNA, and mRNA in LUAD samples and cell lines. Loss-of-function assays were used to evaluate the effects of RP11-89K21.1 on LUAD cell proliferation and gefitinib resistance. Bioinformatics analysis, luciferase reporter assay, and Western blot were employed to explore the regulatory relationships among RP11-89K21.1, miR-146a/b-5p, and RHPN2. Results: The authors identified that RP11-89K21.1 was highly expressed in LUAD tissues and cell lines. Moreover, upregulated RP11-89K21.1 was strongly associated with unfavorable overall survival of patients with LUAD. Knockdown of RP11-89K21.1 significantly suppressed proliferation and sensitized cell to gefitinib. Mechanistically, RP11-89K21.1 could directly bind miR-146a-5p and miR-146b-5p and decrease their expression to upregulate RHPN2, and subsequently activated RhoA/ROCK pathway. More importantly, overexpression of RHPN2 reversed regulatory effects of RP11-89K21.1 knockdown on cell proliferation and gefitinib resistance. Conclusions: These observations provide new insights into the role of RP11-89K21.1 in regulating LUAD tumorigenesis, suggesting that RP11-89K21.1 is a potential therapeutic target for LUAD treatment.
Annotations
External Annotation for RP11-89K21.1 |
|
|---|---|
 |
LncRNA-associated competing triplets and functions. |
 |
Comprehensive experimentally supported associations between lncRNA and human cancer. |
 |
Infer genomic variations that disturb lncRNA-associated ceRNA regulation.. |
 |
Provide and annotate disease or phenotype-associated variants in human long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs) or their regulatory elements. |
 |
Providing cellular-specific lncRNA-associated ceRNA networks predicted via high-throughput analysis of single-cell genomic data. |
 |
Information on all annotated and predicted human genes. |
 |
Gene nomenclature, gene families and associated resources (genomic, proteomic, phenotypic information). |
 |
Genome browser for vertebrate genomes. |
 |
An annotated collection of all publicly available DNA sequences. |
 |
A wiki-based platform for community curation of human long non-coding RNAs. |
 |
An integrated knowledge database dedicated to non-coding RNAs. |
 |
An integrated database of human annotated lncRNA transcripts. |
 |
Comprehensive annotations of eukaryotic long non-coding RNAs. |
 |
Comprehensive experimentally supported associations between lncRNA and human cancer. |
 |
A comprehensive, authoritative compendium of human genes and genetic phenotypes. |
 |
The catalogue of somatic mutations in cancer. |
