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• Non-coding RNA: what is functional and what is junk?

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WebPage:
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         headline:METTL1 mediated tRNA m7G modification promotes leukaemogenesis of AML via tRNA regulated translational control
         description:RNA modifications have been proven to play fundamental roles in regulating cellular biology process. Recently, maladjusted N7-methylguanosine (m7G) modification and its modifiers METTL1/WDR4 have been confirmed an oncogene role in multiple cancers. However, the functions and molecular mechanisms of METTL1/WDR4 in acute myeloid leukemia (AML) remain to be determined. METTL1/WDR4 expression levels were quantified using qRT-PCR, western blot analysis on AML clinical samples, and bioinformatics analysis on publicly available AML datasets. CCK-8 assays and cell count assays were performed to determine cell proliferation. Flow cytometry assays were conducted to assess cell cycle and apoptosis rates. Multiple techniques were used for mechanism studies in vitro assays, such as northern blotting, liquid chromatography-coupled mass spectrometry (LC–MS/MS), tRNA stability analysis, transcriptome sequencing, small non-coding RNA sequencing, quantitative proteomics, and protein synthesis measurements. METTL1/WDR4 are significantly elevated in AML patients and associated with poor prognosis. METTL1 knockdown resulted in reduced cell proliferation and increased apoptosis in AML cells. Mechanically, METTL1 knockdown leads to significant decrease of m7G modification abundance on tRNA, which further destabilizes tRNAs and facilitates the biogenesis of tsRNAs in AML cells. In addition, profiling of nascent proteins revealed that METTL1 knockdown and transfection of total tRNAs that were isolated from METTL1 knockdown AML cells decreased global translation efficiency in AML cells. Taken together, our study demonstrates the important role of METTL1/WDR4 in AML leukaemogenesis, which provides a promising target candidate for AML therapy.
         datePublished:2024-01-24T00:00:00Z
         dateModified:2024-01-24T00:00:00Z
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            Hematology
            Oncology
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      headline:METTL1 mediated tRNA m7G modification promotes leukaemogenesis of AML via tRNA regulated translational control
      description:RNA modifications have been proven to play fundamental roles in regulating cellular biology process. Recently, maladjusted N7-methylguanosine (m7G) modification and its modifiers METTL1/WDR4 have been confirmed an oncogene role in multiple cancers. However, the functions and molecular mechanisms of METTL1/WDR4 in acute myeloid leukemia (AML) remain to be determined. METTL1/WDR4 expression levels were quantified using qRT-PCR, western blot analysis on AML clinical samples, and bioinformatics analysis on publicly available AML datasets. CCK-8 assays and cell count assays were performed to determine cell proliferation. Flow cytometry assays were conducted to assess cell cycle and apoptosis rates. Multiple techniques were used for mechanism studies in vitro assays, such as northern blotting, liquid chromatography-coupled mass spectrometry (LC–MS/MS), tRNA stability analysis, transcriptome sequencing, small non-coding RNA sequencing, quantitative proteomics, and protein synthesis measurements. METTL1/WDR4 are significantly elevated in AML patients and associated with poor prognosis. METTL1 knockdown resulted in reduced cell proliferation and increased apoptosis in AML cells. Mechanically, METTL1 knockdown leads to significant decrease of m7G modification abundance on tRNA, which further destabilizes tRNAs and facilitates the biogenesis of tsRNAs in AML cells. In addition, profiling of nascent proteins revealed that METTL1 knockdown and transfection of total tRNAs that were isolated from METTL1 knockdown AML cells decreased global translation efficiency in AML cells. Taken together, our study demonstrates the important role of METTL1/WDR4 in AML leukaemogenesis, which provides a promising target candidate for AML therapy.
      datePublished:2024-01-24T00:00:00Z
      dateModified:2024-01-24T00:00:00Z
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         METTL1/WDR4
         tRNA modification
         m7G
         AML
         Translation control
         Hematology
         Oncology
         Cancer Research
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PostalAddress:
      name:Medical Center of Hematology, Xinqiao Hospital of Army Medical University, Chongqing, China
      name:Department of Hematology, Affiliated Hospital of North Sichuan Medical College, Nanchong, China
      name:Medical Center of Hematology, Xinqiao Hospital of Army Medical University, Chongqing, China
      name:Medical Center of Hematology, Xinqiao Hospital of Army Medical University, Chongqing, China
      name:Medical Center of Hematology, Xinqiao Hospital of Army Medical University, Chongqing, China
      name:Medical Center of Hematology, Xinqiao Hospital of Army Medical University, Chongqing, China
      name:Medical Center of Hematology, Xinqiao Hospital of Army Medical University, Chongqing, China
      name:Medical Center of Hematology, Xinqiao Hospital of Army Medical University, Chongqing, China
      name:Medical Center of Hematology, Xinqiao Hospital of Army Medical University, Chongqing, China
      name:Medical Center of Hematology, Xinqiao Hospital of Army Medical University, Chongqing, China
      name:Clinical and Translational Research Center of Shanghai First Maternity and Infant Hospital, Shanghai Key Laboratory of Signaling and Disease Research, Frontier Science Center for Stem Cell Research, School of Life Sciences and Technology, Tongji University, Shanghai, China
      name:Medical Center of Hematology, Xinqiao Hospital of Army Medical University, Chongqing, China
      name:Chongqing Key Laboratory of Hematology and Microenvironment, Chongqing, China
      name:State Key Laboratory of Trauma and Chemical Poisoning, Chongqing, China

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