ArticleMolecular therapy. Nucleic acids2025
RNA splicing variants of the novel long non-coding RNA, CyKILR, possess divergent biological functions in non-small cell lung cancer.
Article in Molecular therapy. Nucleic acids, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed.
- The lncRNA, CyKILRb acts as a ceRNA for tumor suppressive microRNA to augment oncogenic phenotype via induction of PIK3R2/PIMolecular therapy. Nucleic acids · 2026Article
- Establishment and characterization of an orthotopic implanted lung cancer model to mimic human tumor structure, microenvironment, and metastatic spread.Translational lung cancer research · 2025Article
- CyKILR splice variants: A double-edged sword in non-small cell lung cancer.Molecular therapy. Nucleic acids · 2025Article
- Role of lncRNAs in pathophysiology of obesity.Current opinion in physiology · 2025Article
- Long Non-Coding RNAs: Key Regulators of Tumor Epithelial/Mesenchymal Plasticity and Cancer Stemness.Cells · 2025Review
- Future horizons in diabetes treatment: hypoglycemic activity of [1,2,4]triazino[2,3-Frontiers in endocrinology · 2025Article
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Abstract
The CDKN2A gene, responsible for encoding the tumor suppressors p16(INK4A) and p14(ARF), is frequently inactivated in non-small cell lung cancer (NSCLC). Herein, an uncharacterized long non-coding RNA (lncRNA) (ENSG00000267053) on chromosome 19p13.12 was found to be overexpressed in NSCLC cells with an active, wild-type CDKN2A gene. This lncRNA, named cyclin-dependent kinase inhibitor 2A-regulated lncRNA (CyKILR), also correlated with an active WT STK11 gene, which encodes the tumor suppressor, liver kinase B1. CyKILR displayed two splice variants, CyKILRa (exon 3 included) and CyKILRb (exon 3 excluded), which are cooperatively regulated by CDKN2A and STK11 as knockdown of both tumor suppressor genes was required to induce a significant loss of exon 3 inclusion in mature CyKILR RNA. CyKILRa localized to the nucleus, and its downregulation using antisense RNA oligonucleotides enhanced cellular proliferation, migration, clonogenic survival, and tumor incidence. In contrast, CyKILRb localized to the cytoplasm, and its downregulation using small interfering RNA reduced cell proliferation, migration, clonogenic survival, and tumor incidence. Transcriptomics analyses revealed the enhancement of apoptotic pathways with concomitant suppression of key cell-cycle pathways by CyKILRa demonstrating its tumor-suppressive role. CyKILRb inhibited tumor suppressor miRNAs indicating an oncogenic nature. These findings elucidate the intricate roles of lncRNAs in cell signaling and tumorigenesis.
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