PHAROH lncRNA regulates c-Myc translation in hepatocellular carcinoma via sequestering TIAR
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA704277 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13768436.fastq.gz | Fastqsanger.gz | |||
| SRR13768437.fastq.gz | Fastqsanger.gz | |||
| SRR13768438.fastq.gz | Fastqsanger.gz | |||
| SRR13768439.fastq.gz | Fastqsanger.gz |
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Project description:Hepatocellular carcinoma, the most common type of liver malignancy, is one of the most lethal forms of cancer. We identified a long non-coding RNA, Gm19705, that is over-expressed in hepatocellular carcinoma and mouse embryonic stem cells. We named this RNA Pluripotency and Hepatocyte Associated RNA Overexpressed in HCC, or PHAROH. Depletion of PHAROH impacts cell proliferation and migration, which can be rescued by ectopic expression of PHAROH. RNA-seq analysis of PHAROH knockouts revealed that a large number of genes with decreased expression contain a c-Myc motif in their promoter. C-MYC is decreased at the protein level, but not the mRNA level. RNA-antisense pulldown identified nucleolysin TIAR, a translational repressor, to bind to a 71-nt hairpin within PHAROH, sequestration of which increases c-MYC translation. In summary, our data suggest that PHAROH regulates c-MYC translation by sequestering TIAR and as such represents a potentially exciting diagnostic or therapeutic target in hepatocellular carcinoma.
2021-05-09 | GSE167316 | GEO
Project description:Hepatocellular carcinoma, the most common type of liver malignancy, is one of the most lethal forms of cancer. We identified a long non-coding RNA, Gm19705, that is overexpressed in hepatocellular carcinoma and mouse embryonic stem cells. We named this RNA Pluripotency and Hepatocyte Associated RNA Overexpressed in HCC, or PHAROH. Depletion of PHAROH impacts cell proliferation and migration, which can be rescued by ectopic expression of PHAROH. RNA-seq analysis of PHAROH knockouts revealed that a large number of genes with decreased expression contain a Myc motif in their promoter. MYC is decreased in knockout cells at the protein level, but not the mRNA level. RNA-antisense pulldown identified nucleolysin TIAR, a translational repressor, to bind to a 71-nt hairpin within PHAROH, sequestration of which increases MYC translation. In summary, our data suggest that PHAROH regulates MYC translation by sequestering TIAR and as such represents a potentially exciting diagnostic or therapeutic target in hepatocellular carcinoma.
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Project description:METTL16 was previously identified as an m6A methyltransferase. In this study, we validated the cytoplasmic location of METTL16 and explored its function in the cytoplasm. We found that METTL16 promoted translation by sequestering eIF4E2, a translation initiation repressor, from the 5' cap structure.
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Project description:We report that MYC controls the translation of specific mRNAs in a sequence and RNA binding protein dependent manner. Specifically, using transcriptome-scale ribosome footprinting we identify 882 mRNAs whose translation depends on MYC. These mRNAs are highly significantly enriched for specific 5ÕUTR sequence motifs that bind the SRSF1/RBM42/HNRNPK complex. For example, MYC and SRFSF1/RBM42 dependent transcripts include many components of the electron transport chain and directly affect cellular respiration. Our results provide an integrated map of MYC driven gene expression programs that includes MYCÕs ability to control mRNA translation.
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Project description:To identify proteomic signatures associated with hepatocellular carcinoma driven by MYC overexpression, proteomics was performed on the LAP-tTA/tetO-MYC mouse conditional liver cancer model. Upon MYC activation, mice form liver cancer. Differential proteomics was performed in "MYC on" (MYC-HCC) mouse liver tumors versus mouse control normal liver tissue (where MYC was not overexpressed to drive tumorigenesis -- "MYC off").
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Project description:RNA was isolated from material that had been subjected to immunoprecipitation (IP) from RKO cells that were either left untreated or irradiated with 20 J/m2 UVC and collected 1h later; IP assays were carried out using either an antibody recognizing RNA-binding protein TIAR, or using a control IgG1 antibody. RNA was reverse-transcribed in the presence of [alpha-33P]dCTP and the radiolabeled product used to hybridize human cDNA arrays. The experiment was repeated using three independent sample sets. The samples were numbered Tc-1, Tc-2, Tc-3, Tuv-1, Tuv-2, Tuv-3, IgG1c-1, IgG1c-2, IgG1c-3, IgG1uv-1, IgG1uv-2, and IgG1uv-3. âTcâ denotes RNA from IP reactions using untreated cells and anti-TIAR antibody, âTuvâ denotes RNA from IP reactions using UVC-treated cells and anti-TIAR antibody, âIgG1câ denotes RNA from IP reactions using untreated cells and anti-IgG1 antibody, and âIgG1uvâ denotes RNA from IP reactions using UVC-treated cells and anti-IgG1 antibody. The numbers 1, 2 and 3 correspond to the three independent experimental datasets. Keywords = post-transcriptional / translation / nascent protein synthesis / stress response / ribonomics Keywords: ordered
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Project description:Long non-coding RNAs (lncRNAs) are best known for playing diverse roles at transcriptional level. Here we report a lncRNA MT1JP for its posttranscriptional function as a modulator of tumorigenesis. By associating with RNA-binding protein TIAR, MT1JP favored the translation of vital transcription factor p53, and then regulated a series of p53 involved pathways such as cell cycle, apoptosis, proliferation and so forth. With down-regulation of MT1JP, the protein level of p53 was declined, which in turn accelerated cell deteriorate and tumor formation. Moreover, differential expression of MT1JP in tumor tissues and matched normal tissues suggests that it may be an excellent prognosis and therapy target as a tumor suppressor. Together, our finding identifies MT1JP as a critical lncRNA required for restraining tumorigenesis, which occurs through MT1JP interacting with TIAR to modulate p53 translation.
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Project description:Hepatocellular carcinoma is generally refractory to clinical treatment. Here, we report that inactivation of the MYC oncogene is sufficient to induce sustained regression of invasive liver cancers. MYC inactivation resulted en masse in tumour cells differentiating into hepatocytes and biliary cells forming bile duct structures, and this was associated with rapid loss of expression of the tumour marker alpha-fetoprotein, the increase in expression of liver cell markers cytokeratin 8 and carcinoembryonic antigen, and in some cells the liver stem cell marker cytokeratin 19. Using in vivo bioluminescence imaging we found that many of these tumour cells remained dormant as long as MYC remain inactivated; however, MYC reactivation immediately restored their neoplastic features. Using array comparative genomic hybridization we confirmed that these dormant liver cells and the restored tumour retained the identical molecular signature and hence were clonally derived from the tumour cells. Our results show how oncogene inactivation may reverse tumorigenesis in the most clinically difficult cancers. Oncogene inactivation uncovers the pluripotent capacity of tumours to differentiate into normal cellular lineages and tissue structures, while retaining their latent potential to become cancerous, and hence existing in a state of tumour dormancy. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Using regression correlation
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