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Keywords {🔍}

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Topics {✒️}

meral beksac rip-seq signal surrounding merip-seq hnrnpa2b1/m6a/ilf3/akt3 axis plays ye yang rna-binding protein hnrnp view rna-seq analyses nod-scid mice injected shrna-mediated ilf3 repression high-risk mm marker rip-seq multiple myeloma hnrnpa2b1 accelerating tumor growth enhancing ilf3-mediated expression article download pdf important m6a/hnrnpa2b1 targets original author hnrnp a2 rna metabolism exquisitely promotes mm progression anti-ilf3 antibody confirmed privacy choices/manage cookies rip-qpcr assay frequent rna modifications dynamic rna modifications facilitates tumor growth chunyan gu ilf3-dependent pattern author ilf3 transcript binding natural science foundation rna immunoprecipitation-sequencing m6a-dependent stabilization cellular proliferation induced full size image providing technical support mm cell growth apoptosis assay showed creative commons licence m6a-dependent effect normal plasma cells nat rev genet m6a consensus sequence fenghuang zhan natural product moracin anti-ilf3 antibody editor n6-methyladenosine animal ethics committee hovon65 patient cohorts

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         headline:HNRNPA2B1 promotes multiple myeloma progression by increasing AKT3 expression via m6A-dependent stabilization of ILF3 mRNA
         description:N6-methyladenosine (m6A) modification is the most prevalent modification in eukaryotic RNAs while accumulating studies suggest that m6A aberrant expression plays an important role in cancer. HNRNPA2B1 is a m6A reader which binds to nascent RNA and thus affects a perplexing array of RNA metabolism exquisitely. Despite unveiled facets that HNRNPA2B1 is deregulated in several tumors and facilitates tumor growth, a clear role of HNRNPA2B1 in multiple myeloma (MM) remains elusive. Herein, we analyzed the function and the regulatory mechanism of HNRNPA2B1 in MM. We found that HNRNPA2B1 was elevated in MM patients and negatively correlated with favorable prognosis. The depletion of HNRNPA2B1 in MM cells inhibited cell proliferation and induced apoptosis. On the contrary, the overexpression of HNRNPA2B1 promoted cell proliferation in vitro and in vivo. Mechanistic studies revealed that HNRNPA2B1 recognized the m6A sites of ILF3 and enhanced the stability of ILF3 mRNA transcripts, while AKT3 downregulation by siRNA abrogated the cellular proliferation induced by HNRNPA2B1 overexpression. Additionally, the expression of HNRNPA2B1, ILF3 and AKT3 was positively associated with each other in MM tissues tested by immunohistochemistry. In summary, our study highlights that HNRNPA2B1 potentially acts as a therapeutic target of MM through regulating AKT3 expression mediated by ILF3-dependent pattern.
         datePublished:2021-04-01T00:00:00Z
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      headline:HNRNPA2B1 promotes multiple myeloma progression by increasing AKT3 expression via m6A-dependent stabilization of ILF3 mRNA
      description:N6-methyladenosine (m6A) modification is the most prevalent modification in eukaryotic RNAs while accumulating studies suggest that m6A aberrant expression plays an important role in cancer. HNRNPA2B1 is a m6A reader which binds to nascent RNA and thus affects a perplexing array of RNA metabolism exquisitely. Despite unveiled facets that HNRNPA2B1 is deregulated in several tumors and facilitates tumor growth, a clear role of HNRNPA2B1 in multiple myeloma (MM) remains elusive. Herein, we analyzed the function and the regulatory mechanism of HNRNPA2B1 in MM. We found that HNRNPA2B1 was elevated in MM patients and negatively correlated with favorable prognosis. The depletion of HNRNPA2B1 in MM cells inhibited cell proliferation and induced apoptosis. On the contrary, the overexpression of HNRNPA2B1 promoted cell proliferation in vitro and in vivo. Mechanistic studies revealed that HNRNPA2B1 recognized the m6A sites of ILF3 and enhanced the stability of ILF3 mRNA transcripts, while AKT3 downregulation by siRNA abrogated the cellular proliferation induced by HNRNPA2B1 overexpression. Additionally, the expression of HNRNPA2B1, ILF3 and AKT3 was positively associated with each other in MM tissues tested by immunohistochemistry. In summary, our study highlights that HNRNPA2B1 potentially acts as a therapeutic target of MM through regulating AKT3 expression mediated by ILF3-dependent pattern.
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      name:Chunyan Gu
      affiliation:
            name:The Third Affiliated Hospital of Nanjing University of Chinese Medicine
            address:
               name:The Third Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China
               type:PostalAddress
            type:Organization
            name:Nanjing University of Chinese Medicine
            address:
               name:School of Medicine and Holistic Integrative Medicine, Nanjing University of Chinese Medicine, Nanjing, China
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Ye Yang
      url:http://orcid.org/0000-0003-0228-5102
      affiliation:
            name:Nanjing University of Chinese Medicine
            address:
               name:School of Medicine and Holistic Integrative Medicine, Nanjing University of Chinese Medicine, Nanjing, China
               type:PostalAddress
            type:Organization
            name:University of Iowa
            address:
               name:Internal Medicine, University of Iowa, Iowa City, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:The Third Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China
      name:School of Medicine and Holistic Integrative Medicine, Nanjing University of Chinese Medicine, Nanjing, China
      name:School of Medicine and Holistic Integrative Medicine, Nanjing University of Chinese Medicine, Nanjing, China
      name:School of Medicine and Holistic Integrative Medicine, Nanjing University of Chinese Medicine, Nanjing, China
      name:School of Medicine and Holistic Integrative Medicine, Nanjing University of Chinese Medicine, Nanjing, China
      name:School of Medicine and Holistic Integrative Medicine, Nanjing University of Chinese Medicine, Nanjing, China
      name:School of Medicine and Holistic Integrative Medicine, Nanjing University of Chinese Medicine, Nanjing, China
      name:School of Medicine and Holistic Integrative Medicine, Nanjing University of Chinese Medicine, Nanjing, China
      name:School of Medicine and Holistic Integrative Medicine, Nanjing University of Chinese Medicine, Nanjing, China
      name:Department of Hematology, Jagiellonian University Medical College, Cracow, Poland
      name:Division of Hematology and Oncology, Medical College of Wisconsin, Milwaukee, USA
      name:Department of Hematology, School of Medicine, Ankara University, Ankara, Turkey
      name:Internal Medicine, University of Iowa, Iowa City, USA
      name:Myeloma Center, University of Arkansas, Little Rock, USA
      name:The Third Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China
      name:School of Medicine and Holistic Integrative Medicine, Nanjing University of Chinese Medicine, Nanjing, China
      name:School of Medicine and Holistic Integrative Medicine, Nanjing University of Chinese Medicine, Nanjing, China
      name:Internal Medicine, University of Iowa, Iowa City, USA

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