miR-218-5p inhibits the malignant progression of glioma via targeting TCF12

Gu, Jingshun; Ge, Xuehua; You, Aiwu; Li, Jun; Zhang, Yuyan; Rao, Guomin; Wang, Juntong; Zhang, Kun; Liu, Xuan; Wu, Xiaotang; Cheng, Ling; Zhu, Meiying; Wang, Dongchun

doi:10.1177/03008916211018263

Cited by 8 publications

(4 citation statements)

References 23 publications

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“…AKAP8 regulates splicing through scaffolding RNAs and RNA processing factors 16 . TCF12, belonging to the basic helix‐loop‐helix (bHLH) subfamily of transcription factors, is known to have a crucial regulatory role in certain types of cancers 31 . CRTC3 plays important roles in adipose development and energy metabolism 32 .…”

Section: Discussionmentioning

confidence: 99%

“…16 TCF12, belonging to the basic helixloop-helix (bHLH) subfamily of transcription factors, is known to have a crucial regulatory role in certain types of cancers. 31 CRTC3 plays important roles in adipose development and energy metabolism. 32 Ectopic expression of CRTC3 in hepatoma cells stimulated the activity of the preS2/S promoter of hepatitis B virus (HBV).…”

Section: The General Mechanism Of Nsp12 Modulate the Cellular Genome Asmentioning

confidence: 99%

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SARS‐CoV‐2 NSP12 utilizes various host splicing factors for replication and splicing regulation

Yang,

Zeng,

Luo

et al. 2024

Journal of Medical Virology

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The RNA‐dependent RNA polymerase (RdRp) is a crucial element in the replication and transcription of RNA viruses. Although the RdRps of lethal human coronaviruses severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2), SARS‐CoV, and Middle East respiratory syndrome coronavirus (MERS‐CoV) have been extensively studied, the molecular mechanism of the catalytic subunit NSP12, which is involved in pathogenesis, remains unclear. In this study, the biochemical and cell biological results demonstrate the interactions between SARS‐CoV‐2 NSP12 and seven host proteins, including three splicing factors (SLU7, PPIL3, and AKAP8). The entry efficacy of SARS‐CoV‐2 considerably decreased when SLU7 or PPIL3 was knocked out, indicating that abnormal splicing of the host genome was responsible for this occurrence. Furthermore, the polymerase activity and stability of SARS‐CoV‐2 RdRp were affected by the three splicing factors to varying degrees. In addition, NSP12 and its homologues from SARS‐CoV and MERS‐CoV suppressed the alternative splicing of cellular genes, which were influenced by the three splicing factors. Overall, our research illustrates that SARS‐CoV‐2 NSP12 can engage with various splicing factors, thereby impacting virus entry, replication, and gene splicing. This not only improves our understanding of how viruses cause diseases but also lays the foundation for the development of antiviral therapies.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: The General Mechanism Of Nsp12 Modulate the Cellular Genome Asmentioning

confidence: 99%

SARS‐CoV‐2 NSP12 utilizes various host splicing factors for replication and splicing regulation

Yang,

Zeng,

Luo

et al. 2024

Journal of Medical Virology

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show abstract

“…AKAP8 regulates splicing through scaffolding RNAs and RNA processing factors [16]. TCF12, belonging to the basic helix-loop-helix (bHLH) subfamily of transcription factors, is known to have a crucial regulatory role in certain types of cancers [31]. CRTC3 plays important roles in adipose development and energy metabolism [32].…”

Section: Discussionmentioning

confidence: 99%

SARS-CoV-2 NSP12 utilizes various host splicing factors for replication and splicing regulation

Yang

Zeng

Ren

et al. 2023

Preprint

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Background The RNA-dependent RNA polymerase (RdRp) is a crucial element in the replication and transcription of RNA viruses. Although the RdRps of lethal human coronaviruses SARS-CoV-2, SARS-CoV, and MARS-CoV have been extensively studied, the molecular mechanism of the catalytic subunit NSP12, which is involved in pathogenesis, remains unclear. Results In this study, the biochemical and cell biological results demonstrate the interactions between SARS-CoV-2 NSP12 and seven host proteins, including three splicing factors (SLU7, PPIL3, and AKAP8), suggesting that the polymerase activity and stability of SARS-CoV-2 RdRp were affected by them to varying degrees. Furthermore, the entry efficacy of SARS-CoV-2 pseudovirus considerably decreased when SLU7 or PPIL3 was knocked out, indicating that abnormal splicing of the host genome was responsible for this occurrence. In addition, NSP12 and its homologues from SARS-CoV and MARS-CoV suppressed thealternative splicing (AS) of cellular genes, which were influenced by the three splicing factors. Conclusions Overall, our research illustrates that SARS-CoV-2 NSP12 can engage with various splicing factors, thereby impacting virus entry, replication, and gene splicing. This not only improves our understanding of how viruses cause diseases but also lays the foundation for the development of antiviral therapies.

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“…Starbase predicted that circFOXM1 had complementary sequence with miR-218-5p. Previous work has suggested the reduction of miR-218-5p level in the tissues of glioma, which was relevant to poor prognosis of patients; and upregulation of miR-218-5p could impede cell proliferative and transferable abilities in glioma by targeting and regulating the expression of TCF12 [11]. However, the action theory of circFOXM1/miR-218-5p axis in glioma progress is indistinct.…”

Section: Introductionmentioning

confidence: 97%

Effect of circFOXM1/miR-218-5p on the proliferation, apoptosis and migration of glioma cells

Renzhi Deng,

Jianying Chen,

Jianying Qin

et al. 2024

Cell Mol Biol (Noisy-le-grand)

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This study aimed to explore the influence of circFOXM1/miR-218-5p molecular axis in the proliferation, apoptosis and migration of glioma cells. The levels of circFOXM1 and miR-218-5p in glioma and adjacent tissues were tested by qRT-PCR. Cultured human glioma U251 cells were randomly split into groups: si-NC, si-circFOXM1, miR-NC, miR-218-5p, si-circFOXM1+anti-miR-NC, si-circFOXM1+anti-miR-218-5p. MTT method, plate clone formation, flow cytometry and Transwell experiments were utilized for detecting the proliferation, clone formation, apoptosis and migration of glioma cells. Dual-luciferase reporter experiment authenticated the targeted relation of circFOXM1 and miR-218-5p. Western blot tested the levels of E-cadherin and N-cadherin. CircFOXM1 was upregulated while miR-218-5p was low expressed in glioma tissues versus normal tissues. After circFOXM1 silence or miR-218-5p overexpression, miR-218-5p level was increased, and cell apoptosis rate and E-cadherin expression were enhancive, whereas cell proliferation, cell clone formation and migration abilities, and N-cadherin level were reduced. CircFOXM1 could affect miR-218-5 level by negative regulation. Furthermore, miR-218-5p silence could reverse the stimulative influence of si-circFOXM1 on apoptosis rate, and E-cadherin level, and the repressive effect on cell viability, cell number of colony formation and migration, and N-cadherin expression. Inhibition of circFOXM1 expression could block the proliferation, clone formation, and migration and induce apoptosis of glioma cells by upregulating miR-218-5p.

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miR-218-5p inhibits the malignant progression of glioma via targeting TCF12

Cited by 8 publications

References 23 publications

SARS‐CoV‐2 NSP12 utilizes various host splicing factors for replication and splicing regulation

SARS‐CoV‐2 NSP12 utilizes various host splicing factors for replication and splicing regulation

SARS-CoV-2 NSP12 utilizes various host splicing factors for replication and splicing regulation

Effect of circFOXM1/miR-218-5p on the proliferation, apoptosis and migration of glioma cells

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