ArticleCytotechnology2025
N6-methyladenosine (m6A) RNA methylation of LncRNA LINC01214 accelerates the progression of non-small cell lung cancer (NSCLC) by targeting miR-195-5p/ROCK1 axis.
Article in Cytotechnology, 2025. 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
Long non-coding RNA LINC01214 is reported to be up-regulated in non-small cell lung cancer (NSCLC), however, its function in NSCLC has not been elucidated yet. In our study, we verified that LINC01214 was aberrantly higher in the tumor tissues and cell lines than that in the normal controls, and was relevant to the severity and prognosis of NSCLC through using real-time quantitative PCR. Then, 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di-phenytetrazoliumromide assay and flow cytometry illustrated that knocking down LINC01214 restrained cell proliferation and promoted apoptosis in A549 and H1299 cells. Additionally, western blot results confirmed that LINC01214 silence reduced the protein expression of CDK2, CDK6, CyclinD1 and Bcl2, but increased the protein expression of Bax and Caspase-3. Of note, compared to normal cells, NSCLC cells had higher enrichment level of N6-methyladenosine (m6A) modification of LINC01214, while reducing m6A modification of LINC01214 weakened the stability of LINC01214 and diminished its level in A549 and H1299 through down-regulating methyltransferase METTL3 or overexpressing demethylase ALKBH5. Subsequently, molecular experiments proved that LINC01214 acted as a sponge for miR-195-5p to elevate ROCK1 expression in NSCLC. Furthermore, data from functional recovery experiments showed that elevating miR-195-5p also exerted tumor-suppressive effects in NSCLC; meanwhile, the effects were reversed by overexpressing ROCK1 or inhibiting miR-195-5p. In short, m6A modification-mediated up-regulation of LINC01214 advances cell proliferation and tumorigenesis to promote NSCLC progression through inhibiting miR-195-5p to up-regulate ROCK1.
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