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Basic Information

Classification Information

Regulatory Mechanism		Biological Function		Clinical Application
TF		Immune		Survival
Enhancer		Apoptosis	apoptosis	Drug	erlotinib
Variant		Cell Growth		Circulating	2
MiRNA		EMT		Metastasis
Methylation		Coding Ability		Recurrence

Cancer&Entry Information

Cancer Name	non small cell lung cancer
ICD-0-3	C34
Methods	Microarray, qPCR, Western blot, in vitro knockdown
Sample	non small cell lung cancer serum samples, cell lines (HCC827 and HCC4006)
Expression Pattern	up-regulated
Function Description	RP11-838N2.4 was upregulated in erlotinib-resistant cells when compared to normal NSCLC cells. Furthermore, bioinformatics analysis and chromatin immunoprecipitation revealed that forkhead box protein O1 (FOXO1) could bind to the promoter region of lncRNA RP11-838N2.4, resulting in its silencing through the recruitment of histone deacetylase. Functional experiments demonstrated that the knockdown of lncRNA RP11-838N2.4 potently promoted erlotinib-induced cytotoxicity. lncRNA RP11-838N2.4 knockdown promoted apoptosis induced by erlotinib treatment in both erlotinib-resistant cell lines. Furthermore, extracellular lncRNA RP11-838N2.4 could be incorporated into exosomes and transmitted to sensitive cells, thus disseminating erlotinib resistance. Treatment-sensitive cells with exosomes containing lncRNA RP11-838N2.4 induced erlotinib resistance, while the knockdown of lncRNA RP11-838N2.4 abrogated this effect. In addition, the serum expression levels of exosomal lncRNA RP11-838N2.4 were upregulated in patients exhibiting resistance to erlotinib treatment.
Pubmed ID	29845246
Year	2018
Title	Exosome-mediated Transfer of lncRNA RP11-838N2.4 Promotes Erlotinib Resistance in Non-Small Cell Lung Cancer

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