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Transcriptomic analysis of the RPS3-regulated genes in HCC cell line

ABSTRACT: The human ribosomal protein S3 (RPS3), a component of the small 40S ribosomal subunit, is mainly involved in ribosomal maturation and initiation of translation through association with initiation factors. In this study, we firstly identified that RPS3 played an important role in HCC progression. We performed RNA sequencing to profile gene expression patterns before and after RPS3 knockdown.

ORGANISM(S): Homo sapiens

PROVIDER: GSE118140 | GEO | 2019/02/01

REPOSITORIES: GEO

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Selective translational control of cellular and viral mRNAs by RPS3 mRNA binding

Project description:RPS3, a universal core component of the 40S ribosomal subunit, interacts with mRNA at the entry channel. Whether RPS3 mRNA-binding contributes to specific mRNA translation and ribosome specialization in mammalian cells is unknown. Here we mutated RPS3 mRNA-contacting residues R116, R146 and K148 and report their impact on cellular and viral translation. R116D weakened cap-proximal initiation and promoted leaky scanning, while R146D had the opposite effect. Additionally, R146D and K148D displayed contrasting effects on start-codon fidelity. Translatome analysis uncovered common differentially translated genes of which the downregulated set bears long 5’UTR and weak AUG context, suggesting a stabilizing role during scanning and AUG selection. We identified an RPS3-dependent regulatory sequence (RPS3RS) in the sub-genomic 5’UTR of SARS-CoV-2 consisting of a CUG initiation codon and a downstream element that is also the viral transcription regulatory sequence (TRS). Furthermore, RPS3 mRNA-binding residues were essential for SARS-CoV-2 NSP1-mediated inhibition of host translation and for its ribosomal binding. Intriguingly, NSP1-induced mRNA degradation was also reduced in R116D cells, indicating that mRNA decay occurs in the ribosome context. Thus, RPS3 mRNA-binding residues have multiple translation regulatory functions and are exploited by SARS-CoV-2 in various ways to influence host and viral mRNA translation and stability.

2023-04-12 | GSE217181 | GEO

Ribosomal protein S3 mediates drug resistance of proteasome inhibitor: therapeutic application in multiple myeloma

Project description:Multiple myeloma (MM) remains incurable due to drug resistance. Ribosomal protein S3 (RPS3) has been identified as a non-Rel subunit of NF-κB. However, the detailed biological roles of RPS3 remain unclear. Here, we report for the first time that RPS3 is necessary for MM survival and drug resistance. RPS3 was highly expressed in MM, and knockout of RPS3 in MM inhibited cell growth and induced cell apoptosis both in vitro and in vivo. Overexpression of RPS3 mediated the proteasome inhibitor resistance of MM and delayed the survival of MM tumour-bearing animals. Moreover, our present study found an interaction between RPS3 and the thyroid hormone receptor interactor 13 (TRIP13), an oncogene related to MM tumorigenesis and drug resistance. We demonstrated that the phosphorylation of RPS3 was mediated by TRIP13 via PKCδ, which played an important role in activating the canonical NF-κB signalling and inducing cell survival and drug resistance in MM. Notably, the inhibition of NF-κB signalling by the small-molecule inhibitor targeting TRIP13, DCZ0415, was capable of triggering synergistic cytotoxicity when combined with bortezomib in drug-resistant MM. This study identifies RPS3 as a novel biomarker and therapeutic target in MM.

2023-08-18 | GSE240978 | GEO

Transcriptomic analysis of the RPS3-regulated genes in HCC cell line

Project description:Transcriptomic analysis of the RPS3-regulated genes in HCC cell line

| PRJNA484691 | ENA

Cleavage mapping in rps3

Project description:Mapping 3'ends of mRNAs from a reporter subject to no-go decay in an rps3 mutant background.

2018-11-09 | GSE117652 | GEO

Ribosomal protein S3 regulates GLI2-mediated osteosarcoma invasion

Project description:It has been reported that GLI2 promotes proliferation, migration, and invasion of mesenchymal stem cell and osteosarcoma cells. To examine the molecular mechanisms of GLI2-mediated osteosarcoma metastasis, we performed a microarray analysis. The gene encoding ribosomal protein S3 (RPS3) was identified as a target of GLI2. Real-time PCR revealed that RPS3 was upregulated in osteosarcoma cell lines compared with normal osteoblast cells. Knockdown of GLI2 decreased RPS3 expression, whereas forced expression of a constitutively active form of GLI2 upregulated the expression of RPS3. RPS3 knockdown by siRNA decreased the migration and invasion of osteosarcoma cells. Although forced expression of constitutively active GLI2 increased the migration of human mesenchymal stem cells, knockdown of RPS3 reduced the up-regulated migration. In contrast, forced expression of RPS3 increased migration and invasion of osteosarcoma cells. Moreover, reduction of migration by GLI2 knockdown was rescued by forced expression of RPS3. Immunohistochemical analysis showed that RPS3 expression was increased in primary osteosarcoma lesions with lung metastases compared with those without. These findings indicate that GLI2–RPS3 signaling may be a marker of invasive osteosarcoma and a therapeutic target for patients with osteosarcoma.

2012-12-14 | GSE42903 | GEO

Cleavage mapping in rps3

Project description:Cleavage mapping in rps3

| PRJNA482833 | ENA

Effect of RPS3 Serine 149 mutation on gene expression in hiPSC-derived cardiomyocytes during Ang II administration

Project description:Angiotensin II (Ang II) treatment contributes to hypertrophic growth and mitochondrial dysfunction in hiPSC-derived cardiomyocytes. Here, we report enhanced RPS3 phosphorylation at serine 149 in nuclear compartment and abnormal mitochondrial biogenesis during Ang II incubation. Furthermore, RPS3 S149 mutation attenuated Ang II induced cardiomyocyte hypertrophy and improved mitochondrial biogenesis and dysfunction. Mechanistically, RPS3 Ser149 mutation promoted mitochondrial RNA stabilization and blunt Ang II induced mitochodnrial RNA alternative splicing for degradation, by which RPS3 dephosphorylation restored mitochondrial complex assembly in cardiomyocytes.

2023-07-30 | GSE238123 | GEO

Semaglutide reduces tumor burden in the GAN diet-induced obese and biopsy-confirmed mouse model of NASH-HCC with advanced fibrosis

Project description:We applied RNA sequencing (RNA-seq) to study the gene expression profile in the liver of GAN DIO-NASH-HCC mice (non-tumorous tissue samples, n=9; tumor samples, n=9) and chow-fed controls (healthy liver samples, n=5)). Comparing tumour tissue of GAN DIO-NASH-HCC mice to healthy chow-fed controls, we find that tumors of GAN DIO-NASH-HCC mice show widespread regulations of genes associated with human HCC. Human HCC can be classified into three categories (S1-S3). Using the human S1-S3 gene classification described by Hoshida Y. et al. (2009), we find that GAN DIO-NASH-HCC tumors resemble the human S1 class of proliferating HCC tumors with poor prognosis.

2024-01-02 | GSE243976 | GEO

Differential miRNA expression profiles betweenHBV-related HCC tumor versus non-tumor liver tissue

Project description:miRNA played an important role in the process of carcinogenesis in HBV related hepatocellular carcinoma. Therefore, we performed miRNA microarray to evaluate the miRNAs that expressed differentially between HCC tumor versus non-tumor liver tissues. RNA was extracted from snap fresh tissue collected from resected HCC tumor and adjacent non-tumor liver tissues. All HCC tumors were HBV-associated HCC.

2015-07-22 | E-GEOD-69580 | biostudies-arrayexpress

Transcriptome analysis in hepatocellular carcinoma (HCC) tissues

Project description:We report the application of RNA sequencing technology for high-throughput profiling in HCC tissues. In the present study, to explore novel biomarkers of HCC, we firstly explored the expression profiles of mRNAs and miRNAs in three pairs of HCC patients (tumor tissues and non-tumorous tissues) by high-throughput RNA sequencing. A total of 1024 mRNAs were found to be significantly dysregulated (636 up-regulated and 388 down-regulated), 50 miRNAs were found to be significantly dysregulated (27 up-regulated and 23 down-regulated) in the HCC tissues compared with the non-tumorous tissues.Then validae the differentially expressed miRNAs by qRT-PCR in HCC tissues and serum. This study provides a framework for the application of miRNAs to be ideal biomarkers for HCC.

2023-02-28 | GSE146719 | GEO

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