METTL14 suppresses cancer stem cell phenotype of colorectal cancer via regulating of β-catenin/NANOG

Sun, Chuanyu; Chen, Jiong; Xing, Zhichen; Guo, Tao

doi:10.7150/jca.82158

Cited by 2 publications

References 53 publications

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m6A reader YTHDF1 inhibits the growth of neuroblastoma in vitro and in vivo

Deng

Long

Yang³

et al. 2023

Preprint

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Purpose Neuroblastoma (NB) is the most common extracranial solid tumor in childhood, always leading to an unfavorable prognosis. m6A is the most prevalent modification in eukaryotic RNAs. Util now, the role of N6-methyladenosine (m6A) in NB has not been elucidated. In this study, we aim to explore the role of m6A reader YTHDF1 in regulating NB proliferation and growth in vitro and in vivo.Methods We evaluate the role of YTHDF1 in mediating NB cell growth using in vitro and in vivo methods. We perform immunohistochemistry assay to detect the expression of YTHDF1 in NB clinical samples. Cell proliferation assay was used to test the growth of NB cell line. The tumor xenograft mouse model was performed to evaluate the role of YTHDF1 in vivo. RNA-seq was applied to uncover the genes that changed upon YTHDF1 knockdown.Results Our results showed that the expression of YTHDF1 is significantly increased in clinical neuroblastoma samples compared with that of ganglioneuroma (GN) and ganglioneuroblastoma (GNB). Cellular assays demonstrated that knockdown of YTHDF1 inhibits NB cell growth and proliferation. The tumor xenograft mouse model suggests that knockdown of YTHDF1 suppresses the growth of neuroblastoma in vivo. RNA-seq showed that the expression of a series genes was changed upon YTHDF1 knockdown, including ACER3, WNT2B and ANKRD62.Conclusion In conclusion, our study provides a new therapeutic target for the treatment of neuroblastoma via inhibiting YTHDF1.

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m6A reader YTHDF1 inhibits the growth of neuroblastoma in vitro and in vivo

Deng

Long

Yang³

et al. 2023

Preprint

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Combating cancer stem cells: RNA m6A methylation and small-molecule drug discovery

Zhang,

Wang,

Chen

et al. 2024

Front. Drug Discov.

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Cancer stem cells (CSCs) are a small population of less differentiated cells with robust self-renewal ability. CSCs have been recognized as the root cause of tumor initiation, progression, relapse, and drug resistance. Recent studies from us and others have highlighted that N6-methyladenosine (m6A), the most prevalent modification in mRNA, plays a crucial role in carcinogenesis and CSC homeostasis. Dysregulation of the m6A modification machinery has been implicated in CSC survival and self-renewal, thereby regulating cancer progression and therapeutic resistance. In this review, we provide an overview of the roles and molecular mechanisms of the RNA m6A modification machinery in CSC survival and self-renewal. Additionally, we summarize the currently known small-molecule inhibitors targeting the dysregulated m6A modification machinery and discuss proof-of-concept studies focusing on the efficacy of these compounds in eliminating CSCs and cancers.

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METTL14 suppresses cancer stem cell phenotype of colorectal cancer via regulating of β-catenin/NANOG

Cited by 2 publications

References 53 publications

m6A reader YTHDF1 inhibits the growth of neuroblastoma in vitro and in vivo

m6A reader YTHDF1 inhibits the growth of neuroblastoma in vitro and in vivo

Combating cancer stem cells: RNA m6A methylation and small-molecule drug discovery

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