ArticleMolecular biotechnology2024
LncRNA RP11-93B14.5 promotes gastric cancer cell growth through PI3K/AKT signaling pathway.
Article in Molecular biotechnology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 3 citations in OpenAlex.
- Regulation of miR-27a-3p/FBXW7 axis by increasing the level of lncRNA AC138128.1 to mitigate gastric cancer progression.World journal of surgical oncology · 2026Article
- Integrative bioinformatics analyses identify EDNRA and BCL2L1 as candidate hub genes linking predicted MEHP targets and gastric cancer.Discover oncology · 2026Article
- LncRNA in gastric cancer drug resistance: deciphering the therapeutic strategies.Frontiers in oncology · 2025Review
- Overexpression of S100 Calcium-Binding Protein A2 is Associated With Poor Prognosis in Hepatocellular Carcinoma.Cancer control : journal of the Moffitt Cancer CenterArticle
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Authors and funding
19 authors at 5 institutions in 1 country.
Funding
Abstract
objectiveEmerging 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.
methodsBioinformatics 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.
resultsBased 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.
conclusionsLncRNA 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.
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