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.

中文翻译：

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m6A 甲基转移酶 METTL14 介导的 RP1-228H13.5 通过靶向 hsa-miR-205/ZIK1 促进肝癌的发生。

本研究的目的是通过生物信息学分析探讨N ⁶ -甲基腺苷（m6A）修饰调控基因相关的长非编码（lnc）RNA RP1-228H13.5与癌症预后的关系，以及RP1-的影响。 228H13.5 关于细胞生物学相关行为和特定分子机制。使用生物信息学分析构建了由九个基因组成的风险模型。该模型可以反映癌症的生存时间和分化程度。随后，构建了一个由 3 个 m6A 相关 lncRNA、6 个 microRNA (miR) 和 201 个 mRNA 组成的竞争性内源 RNA 网络。细胞检测证实RP1-228H13.5在肝癌细胞中显着上调，能够促进肝癌细胞增殖、迁移和侵袭，并抑制肝癌细胞凋亡。具体的分子机制可能是通过靶向下游hsa-miR-205来调节与K蛋白1（ZIK1）相互作用的锌指蛋白的表达。进一步的实验发现 m6A 甲基转移酶 14, N ⁶腺苷甲基转移酶亚基介导 RP1-228H13.5 对 miR-205-5p 表达的调节。m6A 甲基化调节因子相关的 lncRNA 在癌症中具有重要作用。RP1-228H13.5靶向hsa-miR-205调控ZIK1可能是肝癌发生和发展的潜在机制。