Inhibition of lncRNA RPPH1 activity decreases tumor proliferation and metastasis through down-regulation of inflammation-related oncogenes

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Title:	Inhibition of lncRNA RPPH1 activity decreases tumor proliferation and metastasis through down-regulation of inflammation-related oncogenes
Authors:	Lin, Yuan-Ho Chen, Chih-Wei Cheng, Hung-Chi Liu, Chun-Jhih Chung, Sheng-Ting Hsieh, Meng-Che Tseng, Po-Lin Tsai, Wen-Hui Wu, Tian-Shung Lai, Ming-Derg Shih, Chia-Lung Yen, Meng-Chi Fang, Wen-Kuei Chang, Wen-Tsan
Contributors:	Natl Cheng Kung Univ, Inst Basic Med Sci, Coll Med Natl Cheng Kung Univ, Coll Med, Inst Clin Med Chi Mei Med Ctr, Dept Surg Chia Nan Univ Pharm & Sci, Inst Ind Safety & Disaster Prevent, Coll Sustainable Environm, Dept Occupat Safety & Hlth Natl Cheng Kung Univ, Coll Med, Dept Biochem & Mol Biol Chang Gung Univ, Grad Inst Clin Med Sci, Coll Med Chi Mei Fdn Med Ctr, Dept Pediat Chang Jung Christian Univ, Grad Inst Med Sci, Coll Hlth Sci Natl Cheng Kung Univ, Coll Med, Sch Pharm Chia Yi Christian Hosp, Ditmanson Med Fdn, Clin Res Ctr Kaohsiung Med Univ, Dept Emergency Med, Kaohsiung Med Univ Hosp Chia Yi Christian Hosp, Ditmanson Med Fdn, Dept Neurosurg Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Emergency Med Ditmanson Med Fdn, Chia Yi Christian Hosp, Dept Neurosurg Natl Cheng Kung Univ, Coll Med, Inst Basic Med Sci
Keywords:	Long noncoding RNA ribonuclease P RNA component H1 transfer RNA next-generation sequencing tumor progression
Date:	2023
Issue Date:	2024-12-25 11:05:44 (UTC+8)
Publisher:	E-CENTURY PUBLISHING CORP
Abstract:	Objective: Ribonuclease P RNA component H1 (RPPH1) is a long non-coding RNA (lncRNA) associated with cancer progression. Higher RPPH1 expression in breast and cervical cancer samples than that in normal tissues were observed through the lncRNASNP2 database; therefore, silencing RPPH1 expression might be a potential strategy for cancer treatments, even though RPPH1 is also an RNA subunit of ribonuclease P involved in processing transfer RNA (tRNA) precursors and the effect of RPPH1 knockdown is not yet fully understood. Methods: Differentially expressed genes (DEGs) were identified through RNA sequencing in each shRNA-transfected RPPH1 knockdown MDA-MB-231, RPPH1 knockdown HeLa cell, and respective control cells, then the gene ontology enrichment analysis was performed by IPA and MetaCore database according to these DEGs, with further in vitro experiments validating the effect of RPPH1 silencing in MDA-MB-231 and HeLa cells. Results: Hundreds of down -regulated DEGs were identified in RPPH1 knockdown MDA-MB-231 and HeLa cells while bioinformatics analysis revealed that these genes were involved in pathways related to immune response and cancerogenesis. Compared to mock-and vector-transfected cells, the production of mature tRNAs, cell proliferation and migration capacity were inhibited in RPPH1-silenced HeLa and MDA-MB-231 cells. Additionally, RPPH1 knockdown promoted G1 cell cycle arrest mainly through the down-regulation of cyclin D1, although glycolytic pathways were only affected in RPPH1 knockdown HeLa cells but not MDA-MB-231 cells. Conclusion: This study demonstrated that knockdown RPPH1 affected tRNA production, cell proliferation and metabolism. Our findings might provide insight into the role of RPPH1 in tumor development.
Relation:	American Journal of Translational Research, v.15, n.12, pp.6701-6717
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