Transcriptome-wide m6A methylome analysis uncovered the changes of m6A modification in oral pre-malignant cells compared with normal oral epithelial cells
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ABSTRACT:
PROVIDER: PRJNA882098 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21629742_1.fastq.gz | Fastqsanger.gz | |||
| SRR21629742_2.fastq.gz | Fastqsanger.gz | |||
| SRR21629743_1.fastq.gz | Fastqsanger.gz | |||
| SRR21629743_2.fastq.gz | Fastqsanger.gz | |||
| SRR21629744_1.fastq.gz | Fastqsanger.gz |
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Project description:As the most common post-transcriptional RNA modification, m6A methylation extensively regulates the structure and function of RNA. The dynamic and reversible modification of m6A is coordinated by m6A writers and erasers. m6A reader proteins recognize m6A modification on RNA, mediating different downstream biological functions. mRNA m6A modification and its corresponding regulators play an important role in cancers, but its characteristics in the precancerous stage are still unclear. In this study, we used oral precancerous DOK cells as a model to explore the characteristics of transcriptome-wide m6A modification and major m6A regulator expression in the precancerous stage compared with normal oral epithelial cell HOEC and oral cancer cell SCC-9 through MeRIP-seq and RT-PCR. Compared with HOEC cells, we found 1180 hyper-methylated and 1606 hypo-methylated m6A peaks and 354 differentially expressed mRNAs with differential m6A peaks in DOK cells. Although the change of m6A modification in DOK cells was less than that in SCC-9 cells, mRNAs with differential m6A in both cell lines were enriched into many identical GO terms and KEGG pathways. Among the 20 known m6A regulatory genes, FTO, ALKBH5, METTL3 and VIRMA were slightly upregulated or downregulated in DOK cells, but the expression of 10 genes such as METTL14/16, FTO and IGF2BP2/3 changed significantly in SCC-9 cells. Our data suggest that precancerous cells showed, to some extent, changes of m6A modification. Identifying some key m6A targets and corresponding regulators in precancerous stage may provide potential intervention targets for the prevention of cancer development through epigenetic modification in the future.
2022-09-21 | GSE213714 | GEO
Project description:Objective This study aimed to investigate the expression and clinical significance of N6-methyladenosine (m6A) modification of circular RNA (circRNA) in oral leukoplakia (OLK) and oral squamous carcinoma cell (OSCC) tissues. Methods Using methylation RNA immunoprecipitation high-throughput sequencing technology (MeRIP-seq) and RNA high-throughput sequencing technology (RNA-seq), the first circRNA transcriptome analysis for detecting m6A methylationome profiles in OLK and OSCC tissues was obtained, followed by bioinformatics analysis. The qRT-PCR technique and protein immunoblotting technique were used to detect the expression of m6A methylesterase in OLK versus OSCC tissues. Results In this study, 275 differential m6A methylation peaks were identified in OLK and OSCC, among which 193 peaks were up-regulated and 82 were down-regulated. Additionally, 198 differential m6A methylation modified circRNAs were observed, with 127 up-regulated and 71 down-regulated (FC ≥ 2, P < 0.05). Most of the identified circRNAs that underwent m6A methylation alterations were derived from overlapping regions. It was found that the differential expression of circRNAs was not correlated with the joint analysis of significantly different m6A-circRNAs between the two groups. Furthermore, downregulation of mETTL14 and FTO protein levels was observed in OSCC tissues, although there were no discernible alterations in RNA levels. Conclusion Our study suggests that m6A methylation modification of circRNA may play a role in the development of oral leukoplakia, and that METTL14 and FTO may be important methylation enzymes that influence the development of oral leukoplakia. These findings may open up new research directions for in-depth investigations to clarify the molecular mechanisms of OLK carcinogenesis.
2023-09-20 | GSE243097 | GEO
Project description:As the most common post-transcriptional RNA modification, m6A methylation extensively regulates the structure and function of RNA. The dynamic and reversible modification of m6A is coordinated by m6A writers and erasers. m6A reader proteins recognize m6A modification on RNA, mediating different downstream biological functions. mRNA m6A modification and its corresponding regulators play an important role in cancers, but its characteristics in the precancerous stage are still unclear. In this study, we used oral precancerous DOK cells as a model to explore the characteristics of transcriptome-wide m6A modification and major m6A regulator expression in the precancerous stage compared with normal oral epithelial cell HOEC and oral cancer cell SCC-9 through MeRIP-seq and RT-PCR. Compared with HOEC cells, we found 1180 hyper-methylated and 1606 hypo-methylated m6A peaks and 354 differentially expressed mRNAs with differential m6A peaks in DOK cells. Although the change of m6A modification in DOK cells was less than that in SCC-9 cells, mRNAs with differential m6A in both cell lines were enriched into many identical GO terms and KEGG pathways. Among the 20 known m6A regulatory genes, FTO, ALKBH5, METTL3 and VIRMA were upregulated or downregulated in DOK cells, and the expression levels of 10 genes such as METTL14/16, FTO and IGF2BP2/3 were significantly changed in SCC-9 cells. Our data suggest that precancerous cells showed, to some extent, changes of m6A modification. Identifying some key m6A targets and corresponding regulators in precancerous stage may provide potential intervention targets for the prevention of cancer development through epigenetic modification in the future.
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Project description:We report an epitranscriptome-wide mapping of m6A-modified circRNAs (m6A-circRNA) in oral squamous cell carcinoma (OSCC). Utilizing the data of m6A-circRNAs epitranscriptomic microarray analysis, we found that m6A-circRNAs exhibited their particular modification style in OSCC. anti-m6A antibody Synaptic Systems, cat. No. 202003)
2022-07-19 | GSE198105 | GEO
Project description:Glutathione peroxidase 8 (GPX8) is a key regulator of redox homeostasis. Whether its antioxidant activity participates in the regulation of m6A modification is a crucial issue, which has important application value in cancer treatment. MeRIP-seq was used to explore the characteristics of transcriptome-wide m6A modification in GPX8-deficient oral cancer cells in this study. Oxidative stress caused by lack of GPX8 resulted in 1,279 hyper- and 2,287 hypo-methylated m6A peaks and 2,036 differentially expressed genes in GPX8-KO cells. Twenty-eight differentially expressed genes were related to the cell response to oxidative stress, and half of them changed their m6A modification. In GPX8-KO cells, m6A regulators IGF2BP2 and IGF2BP3 were upregulated, while FTO, RBM15, VIRMA, ZC3H13 and YTHDC2 were downregulated. After H2O2 treatment, the expression changes of RBM15, IGF2BP2 and IGF2BP3 were further enhanced. These data indicated that GPX8-mediated redox homeostasis regulated m6A modification, thereby affecting the expression and function of downstream genes. This study highlights the possible significance of GPX8 and the corresponding m6A regulatory or regulated genes as novel targets for antioxidant intervention in cancer therapy
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| 2205076 | ecrin-mdr-crc
Project description:N6-methyladenosine (m6A) is the most prevalent cellular mRNA modification and plays an important role in RNA stability, localization, and gene expression. There are several papers reported that HIV-1 infection upregulates cellular RNA m6A in CD4+ T cells, and this upregulation occurs without changes to the expression levels of the cellular enzymes which add or remove m6A. However, the mechanism of HIV-1 inducing cellular mRNA m6A upregulation is unknown. Here we show that HIV-1 infection upregulates m6A of cellular mRNA and promotes METTL3/METTL14 interaction. We found that HIV-1 infection resulted in increased cellular mRNA m6A level in activated primary CD4+ T cells detected by m6A dot blot and m6A ELISA. We found that HIV-1 infection of CD4+ T cells promotes METTL3/METTL14 interaction compared to mock control using co-immunoprecipitation (co-IP). Our ongoing studies will determine the transcriptomic, epitranscriptomic, and proteomic profiles of CD4+ T cells infected with HIV-1 for 4 days. These studies will facilitate the elucidation of the mechanisms by which HIV-1 infection leads to increased levels of cellular m6A and methyltransferase writers comlex.
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Project description:Here, we profiled N6-methyladenosine (m6A) deposition on nascent RNAs in human cells by a new method MINT-Seq, which revealed that many classes of RTE RNAs, particularly intronic LINE-1s (L1s), are strongly methylated. These m6A-marked intronic L1s (MILs) are evolutionarily young, sense-oriented to hosting genes and nucleate a dozen RNA binding proteins (RBPs) that are putative novel m6A readers, including a nuclear matrix protein SAFB. Notably, m6A positively controls the expression of both autonomous L1s and co-transcribed L1 relics, promoting L1 retrotransposition. We showed that MILs preferentially reside in long genes, where they act as transcriptional ‘roadblock’ to impede the hosting gene expression, revealing a novel host-weakening strategy by the L1s. In counteraction, the host uses the SAFB reader complex to bind m6A-L1s to reduce their levels, and to safeguard hosting gene transcription.
2021-05-14 | GSE137752 | GEO
Project description:Despite effective antiretroviral therapy at reducing HIV-1 viral loads to undetectable levels, the presence of latently infected CD4+ T cells poses a major barrier to HIV-1 cure. N6-methyladenosine (m6A) modification of viral and cellular RNA has a functional role in regulating HIV-1 infection. m6A modification of HIV-1 RNA can affect its stability, translation, and splicing in cells and suppresses type-I interferon induction in macrophages. However, the function of m6A modification in regulating HIV-1 latency reactivation remains unknown. We used the Jurkat T cell line-derived HIV-1 latency model (J-Lat cells) to investigate changes in m6A levels of cellular RNA in response to latency reversal. We observed a significant increase in m6A levels of total cellular RNA upon reactivation of latent HIV-1 in J-Lat cells. This increase in m6A levels was transient and returned to steady-state levels despite continued high levels of viral gene expression in reactivated cells compared to control cells. Upregulation of m6A levels occurred without significant changes in the protein expression of m6A writers or erasers that add or remove m6A, respectively. Knockdown of m6A writers in J-Lat cells significantly reduced HIV-1 reactivation. Treatment of a m6A writer inhibitor reduced cellular RNA m6A levels along with reduction in HIV-1 reactivation. Furthermore, using m6A-specific sequencing, we identified cellular RNAs that are differentially m6A-modified during HIV-1 reactivation in J-Lat cells. Knockdown of identified m6A-modified RNA validate these results with established primary CD4+ T-cell models of HIV-1 latency. These results showed the importance of m6A RNA modification in HIV-1 latency reversal.
2024-10-01 | GSE273614 | GEO
Project description:Expression of m6A methylation-modified circRNA in malignant transformation of oral leukoplakia tissue
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