We are analyzing https://link.springer.com/article/10.1186/s12943-019-1036-9.

Title:
METTL3 promote tumor proliferation of bladder cancer by accelerating pri-miR221/222 maturation in m6A-dependent manner | Molecular Cancer
Description:
Background METTL3 is known to be involved in all stages in the life cycle of RNA. It affects the tumor formation by the regulation the m6A modification in the mRNAs of critical oncogenes or tumor suppressors. In bladder cancer, METTL3 could promote the bladder cancer progression via AFF4/NF-κB/MYC signaling network by an m6A dependent manner. Recently, METTL3 was also found to affect the m6A modification in non-coding RNAs including miRNAs, lincRNAs and circRNAs. However, whether this mechanism is related to the proliferation of tumors induced by METTL3 is not reported yet. Methods Quantitative real-time PCR, western blot and immunohistochemistry were used to detect the expression of METTL3 in bladder cancer. The survival analysis was adopted to explore the association between METTL3 expression and the prognosis of bladder cancer. Bladder cancer cells were stably transfected with lentivirus and cell proliferation and cell cycle, as well as tumorigenesis in nude mice were performed to assess the effect of METTL3 in bladder cancer. RNA immunoprecipitation (RIP), co-immunoprecipitations and RNA m6A dot blot assays were conducted to confirm that METTL3 interacted with the microprocessor protein DGCR8 and modulated the pri-miR221/222 process in an m6A-dependent manner. Luciferase reporter assay was employed to identify the direct binding sites of miR221/222 with PTEN. Colony formation assay and CCK8 assays were conducted to confirm the function of miR-221/222 in METTL3-induced cell growth in bladder cancer. Results We confirmed the oncogenic role of METTL3 in bladder cancer by accelerating the maturation of pri-miR221/222, resulting in the reduction of PTEN, which ultimately leads to the proliferation of bladder cancer. Moreover, we found that METTL3 was significantly increased in bladder cancer and correlated with poor prognosis of bladder cancer patients. Conclusions Our findings suggested that METTL3 may have an oncogenic role in bladder cancer through interacting with the microprocessor protein DGCR8 and positively modulating the pri-miR221/222 process in an m6A-dependent manner. To our knowledge, this is the first comprehensive study that METTL3 affected the tumor formation by the regulation the m6A modification in non-coding RNAs, which might provide fresh insights into bladder cancer therapy.
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Keywords {🔍}

mettl, cancer, bladder, cells, cell, pten, article, expression, google, scholar, knockdown, overexpression, fig, cas, rna, usa, found, tissues, tumor, proliferation, dgcr, significantly, showed, protein, mrna, control, assay, patients, formation, blot, primir, mirnas, decreased, additional, qrtpcr, analysis, performed, colony, increased, data, manner, rnas, western, level, lines, file, study, tumors, assays, mimics,

Topics {✒️}

aff4/nf-κb/myc signaling network aff4/nf-kappab/myc signaling network ji-fu wei cell-type-specific methylation patterns ppp2r2a/akt/mtor axis mettl3/mir221/222/pten regulatory network a-laic-seq reveals targeting mir-146b-5p expression chicken beta-globin locus quantitative real-time pcr article download pdf rna n6-methyladenosine methyltransferase atypical teratoid/rhabdoid tumors kaplan-meier survival curves hmgb1-induced cross talk fine-tuning gene expression kaplan-meier analysis showed n6-methyladenosine-dependent regulation ythdf2-dependent posttranscriptional silencing real-time pcr system full size image anti-β-actin antibody wild-type 3′-utr sequence immunoprecipitated protein-rna complex mettl3-induced cell growth research ethics committee rna methylation regulates cell signaling technology pre-mrna splicing [11 dna-free fragmented rnas privacy choices/manage cookies bladder cancer progression activating wnt signaling cell growth inhibited luciferase reporter assay sv-huc cell methyladenosine-modified rna conjugated secondary antibody ythdf3 facilitates translation full access heterochromatin domain boundaries creative commons license colony formation efficiency paired normal tissues image lab software mesc differentiation potential exhibiting distinct patterns haiwei yang cell proliferation assay glioblastoma stem cells

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WebPage:
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         headline:METTL3 promote tumor proliferation of bladder cancer by accelerating pri-miR221/222 maturation in m6A-dependent manner
         description:METTL3 is known to be involved in all stages in the life cycle of RNA. It affects the tumor formation by the regulation the m6A modification in the mRNAs of critical oncogenes or tumor suppressors. In bladder cancer, METTL3 could promote the bladder cancer progression via AFF4/NF-κB/MYC signaling network by an m6A dependent manner. Recently, METTL3 was also found to affect the m6A modification in non-coding RNAs including miRNAs, lincRNAs and circRNAs. However, whether this mechanism is related to the proliferation of tumors induced by METTL3 is not reported yet. Quantitative real-time PCR, western blot and immunohistochemistry were used to detect the expression of METTL3 in bladder cancer. The survival analysis was adopted to explore the association between METTL3 expression and the prognosis of bladder cancer. Bladder cancer cells were stably transfected with lentivirus and cell proliferation and cell cycle, as well as tumorigenesis in nude mice were performed to assess the effect of METTL3 in bladder cancer. RNA immunoprecipitation (RIP), co-immunoprecipitations and RNA m6A dot blot assays were conducted to confirm that METTL3 interacted with the microprocessor protein DGCR8 and modulated the pri-miR221/222 process in an m6A-dependent manner. Luciferase reporter assay was employed to identify the direct binding sites of miR221/222 with PTEN. Colony formation assay and CCK8 assays were conducted to confirm the function of miR-221/222 in METTL3-induced cell growth in bladder cancer. We confirmed the oncogenic role of METTL3 in bladder cancer by accelerating the maturation of pri-miR221/222, resulting in the reduction of PTEN, which ultimately leads to the proliferation of bladder cancer. Moreover, we found that METTL3 was significantly increased in bladder cancer and correlated with poor prognosis of bladder cancer patients. Our findings suggested that METTL3 may have an oncogenic role in bladder cancer through interacting with the microprocessor protein DGCR8 and positively modulating the pri-miR221/222 process in an m6A-dependent manner. To our knowledge, this is the first comprehensive study that METTL3 affected the tumor formation by the regulation the m6A modification in non-coding RNAs, which might provide fresh insights into bladder cancer therapy.
         datePublished:2019-06-22T00:00:00Z
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            Bladder cancer
            m6A
            miR221/222
            PTEN
            Cancer Research
            Oncology
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      headline:METTL3 promote tumor proliferation of bladder cancer by accelerating pri-miR221/222 maturation in m6A-dependent manner
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         Bladder cancer
         m6A
         miR221/222
         PTEN
         Cancer Research
         Oncology
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