ArticleClinical & experimental metastasis2026
LINC01996 suppresses non-small cell lung cancer proliferation and metastasis by orchestrating the miR-12115/CNRIP1/Ras signaling axis.
Article in Clinical & experimental metastasis, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Lung cancer is the most prevalent cancer and a major cause of cancer-related mortality worldwide. Long non-coding RNAs (lncRNAs) have been confirmed to be dysregulated in the progression of cancers. In this study, through RNA-next generation deep sequencing, we identified a new lncRNA (LINC01996), which was associated with prognosis of non-small cell lung cancer (NSCLC), downregulated in the NSCLC tissues and cell lines. We demonstrated that overexpressing LINC01996 inhibited NSCLC cell proliferation, EMT, and migration. Xenograft mouse models further validated the suppression role of LINC01996 in NSCLC progression and metastasis. By using differentially expressed genes in our RNA-next generation sequencing data, we discovered that LINC01996 was highly correlated with Cannabinoid receptor-interacting protein 1 (CNRIP1). Mechanistically, LINC01996 functions as a competitive endogenous RNA (ceRNA) by sponging miR-12115, thereby alleviating its repressive effect on CNRIP1 and leading to CNRIP1 upregulation. Overexpression of CNRIP1 ultimately inhibited Ras signaling pathway, leading to restrain of NSCLC proliferation and migration. In conclusion, LINC01996 can interact with miR-515-5p in the form of competitive endogenous RNA (ceRNA) to regulate CNRIP1 positively and thus affect the proliferation and metastasis of NSCLC cells. LINC01996/miR-12115/CNRIP1/Ras signaling axis plays a suppressive role in NSCLC progression and metastasis, and could serve as potential diagnostic markers and therapeutic targets for NSCLC.
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