m6A methyltransferase METTL14‑mediated RP1‑228H13.5 promotes the occurrence of liver cancer by targeting hsa‑miR‑205/ZIK1

The aim of the present study was to explore the association between N⁶‑methyladenosine (m6A) modification regulatory gene‑related long noncoding (lnc)RNA RP1‑228H13.5 and cancer prognosis through bioinformatics analysis, as well as the impact of RP1‑228H13.5 on cell biology‑related behaviors and specific molecular mechanisms. Bioinformatics analysis was used to construct a risk model consisting of nine genes. This model can reflect the survival time and differentiation degree of cancer. Subsequently, a competing endogenous RNA network consisting of 3 m6A‑related lncRNAs, six microRNAs (miRs) and 201 mRNAs was constructed. A cell assay confirmed that RP1‑228H13.5 is significantly upregulated in liver cancer cells, which can promote liver cancer cell proliferation, migration and invasion, and inhibit liver cancer cell apoptosis. The specific molecular mechanism may be the regulation of the expression of zinc finger protein interacting with K protein 1 (ZIK1) by targeting the downstream hsa‑miR‑205. Further experiments found that the m6A methyltransferase 14, N⁶‑adenosine‑methyltransferase subunit mediates the regulation of miR‑205‑5p expression by RP1‑228H13.5. m6A methylation regulatory factor‑related lncRNA has an important role in cancer. The targeting of hsa‑miR‑205 by RP1‑228H13.5 to regulate ZIK1 may serve as a potential mechanism in the occurrence and development of liver cancer.