新出现的证据表明，长链非编码RNA（lncRNA）RP11-93B14.5在多种恶性肿瘤中促进肿瘤进展。本研究旨在研究lncRNA RP11-93B14.5在胃癌（GC）中的功能效应及其潜在机制。利用生物信息学分析了GC组织中的lncRNA表达。使用siRNA对GC细胞MKN45和KATO III进行RP11-93B14.5的敲低。利用CRISPR-Cas9构建了稳定的敲低细胞系。利用细胞计数试剂盒-8（CCK-8）测定了GC细胞的存活力。采用软琼脂糖胶块形成实验分析了GC细胞的存活性。采用流式细胞术分析了MKN45和KATO III的细胞周期分布。采用RNA测序（RNA-seq）检测了siRP11-93B14.5转染后的差异基因。采用定量PCR（Q-PCR）检测了GC细胞系的基因表达情况。采用Western-blot分析测量了蛋白质水平。采用RNA荧光原位杂交（FISH）法对lncRNA的细胞定位和表达进行了检测。根据癌症基因组图谱（TCGA）和基因型-组织表达（GTEx）数据库，在GC组织中RP11-93B14.5上调，并与正常胃上皮HFE145细胞相比，在GC细胞系中也得到验证。RP11-93B14.5的敲低降低了MKN45和KATO III细胞的存活力和胞落数，并改变了细胞体外周期分布。RNA-seq分析揭示RP11-93B14.5可能通过S100A2和TIMP2在MKN45和KATO III细胞中调控基因表达。在机制上，RP11-93B14.5可能通过S100A2相关的PI3K/AKT信号通路推动GC的进展。通过调节PI3K/AKT，lncRNA RP11-93B14.5的敲低减轻了GC细胞的恶性表型。我们的结果为lncRNA在调控肿瘤进展中的作用提供了证据。© 2023. 作者，Springer Science+Business Media, LLC, Springer Nature的独家许可。

Emerging evidence indicates that long non-coding RNA (lncRNA) RP11-93B14.5 facilitates tumor progression in variety of malignancies. The present study proposed to study the functional effect of lncRNA RP11-93B14.5 in gastric cancer (GC) as well as the underlying mechanism.Bioinformatics analysis was utilized to analyze lncRNA expression in GC tissues. siRNA was used for knockdown of RP11-93B14.5 in GC cells MKN45 and KATO III. The stable knockdown cell lines were constructed by CRISPR-Cas9. Cell counting kit-8 (CCK-8) assay and soft agar colony formation assay were used to analyze GC cell viability. Flow cytometry analysis was performed to analyze the cell cycle distribution of MKN45 and KATO III. RNA sequencing (RNA-seq) was employed to detect differential genes after transfection with siRP11-93B14.5. Quantitative PCR (Q-PCR) was used to examine gene expression in GC cell lines. Western-blot assay was used to measure protein levels. RNA fluorescent in situ hybridization (FISH) was conducted for lncRNA cellular location and expression.Based on the Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) database, RP11-93B14.5 was upregulated in GC tissue, which was also verified in GC cell lines in comparison to the normal gastric epithelial HFE145 cells. Knockdown of RP11-93B14.5 decreased cell viability and the colony number of MKN45 and KATO III cells, and altered cell cycle distribution in vitro. RNA-seq analysis revealed RP11-93B14.5 may modulate genes expression of S100A2 and TIMP2 in MKN45 and KATO III cells. Mechanistically, RP11-93B14.5 may drive the progression of GC via S100A2 related-PI3K/AKT signaling pathway.LncRNA RP11-93B14.5 knockdown alleviated the malignant phenotypes of GC cells through regulating PI3K/AKT. Our results provide evidence for the role of lncRNAs in regulating tumor progression.© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.