YTHDC1-mediated VPS25 regulates cell cycle by targeting JAK-STAT signaling in human glioma cells

Zhu, Xiaolong; Yang, Hui; Zhang, Mengying; Wu, Xiang; Jiang, Lan; Liu, Xiaocen; Lv, Kun

doi:10.1186/s12935-021-02304-0

Cited by 28 publications

(24 citation statements)

References 71 publications

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“…Meanwhile, VPS25 induced a G0/G1 phase arrest of the cell cycle in glioma cells by directly mediating p21, CDK2, and cyclin E expression, and JAK-signal transducer and activator of transcription (STAT) activation. These results suggest that VPS25 is a promising prognostic indicator and a potential therapeutic target for glioma (Zhu et al, 2021).…”

Section: Janus Kinase/signal Transducer and Activator Of Transcriptio...mentioning

confidence: 69%

“…Signaling cross-talk between JAK/STAT and other pathways is an intricate and colossal network, happens at different levels, and covers varieties of molecules, such as a ligand, receptor, phosphorylation, JAK, STAT, and gene transcription factors etc. (Zhu et al, 2021). These cross-talk activities play crucial roles in pluripotency and differentiation transcription program, immune regulation, and tumorigenesis.…”

Section: Signaling Cross-talk Between Janus Kinase/signal Transducer ...mentioning

confidence: 99%

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Research Progress on the Regulation Mechanism of Key Signal Pathways Affecting the Prognosis of Glioma

Wei

et al. 2022

Front. Mol. Neurosci.

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As is known to all, glioma, a global difficult problem, has a high malignant degree, high recurrence rate and poor prognosis. We analyzed and summarized signal pathway of the Hippo/YAP, PI3K/AKT/mTOR, miRNA, WNT/β-catenin, Notch, Hedgehog, TGF-β, TCS/mTORC1 signal pathway, JAK/STAT signal pathway, MAPK signaling pathway, the relationship between BBB and signal pathways and the mechanism of key enzymes in glioma. It is concluded that Yap1 inhibitor may become an effective target for the treatment of glioma in the near future through efforts of generation after generation. Inhibiting PI3K/Akt/mTOR, Shh, Wnt/β-Catenin, and HIF-1α can reduce the migration ability and drug resistance of tumor cells to improve the prognosis of glioma. The analysis shows that Notch1 and Sox2 have a positive feedback regulation mechanism, and Notch4 predicts the malignant degree of glioma. In this way, notch cannot only be treated for glioma stem cells in clinic, but also be used as an evaluation index to evaluate the prognosis, and provide an exploratory attempt for the direction of glioma treatment. MiRNA plays an important role in diagnosis, and in the treatment of glioma, VPS25, KCNQ1OT1, KB-1460A1.5, and CKAP4 are promising prognostic indicators and a potential therapeutic targets for glioma, meanwhile, Rheb is also a potent activator of Signaling cross-talk etc. It is believed that these studies will help us to have a deeper understanding of glioma, so that we will find new and better treatment schemes to gradually conquer the problem of glioma.

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Section: Janus Kinase/signal Transducer and Activator Of Transcriptio...mentioning

confidence: 69%

Section: Signaling Cross-talk Between Janus Kinase/signal Transducer ...mentioning

confidence: 99%

Research Progress on the Regulation Mechanism of Key Signal Pathways Affecting the Prognosis of Glioma

Wei

et al. 2022

Front. Mol. Neurosci.

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“…YTHDC1 modulates MCM complex-mediated DNA replication and promotes leukemogenesis [ 16 ]. However, YTHDC1 was reported to suppress the progression of glioma by inhibiting VPS25 [ 41 ]. Moreover, YTHDC1 was also found to inhibit glycolysis in pancreatic cancer through the miR-30d/RUNX1 axis [ 42 ].…”

Section: Discussionmentioning

confidence: 99%

YTHDC1 is downregulated by the YY1/HDAC2 complex and controls the sensitivity of ccRCC to sunitinib by targeting the ANXA1-MAPK pathway

et al. 2022

J Exp Clin Cancer Res

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Background Tyrosine kinase inhibitors (TKIs) such as sunitinib are multitarget antiangiogenic agents in clear cell renal cell carcinoma (ccRCC). They are widely used in the treatment of advanced/metastatic renal cancer. However, resistance to TKIs is common in the clinic, particularly after long-term treatment. YTHDC1 is the main nuclear reader protein that binds with m6A to regulate the splicing, export and stability of mRNA. However, the specific role and corresponding mechanism of YTHDC1 in renal cancer cells are still unclear. Methods The Cancer Genome Atlas (TCGA) dataset was used to study the expression of YTHDC1 in ccRCC. Cell counting kit-8 (CCK-8), wound healing, Transwell and xenograft assays were applied to explore the biological function of YTHDC1 in ccRCC. Western blot, quantitative real time PCR (RT‒qPCR), RNA immunoprecipitation PCR (RIP-qPCR), methylated RIP-qPCR (MeRIP-qPCR) and RNA sequencing (RNA-seq) analyses were applied to study the YY1/HDAC2/YTHDC1/ANXA1 axis in renal cancer cells. The CCK-8 assay and xenograft assay were used to study the role of YTHDC1 in determining the sensitivity of ccRCC to sunitinib. Results Our results demonstrated that YTHDC1 is downregulated in ccRCC tissues compared with normal tissues. Low expression of YTHDC1 is associated with a poor prognosis in patients with ccRCC. Subsequently, we showed that YTHDC1 inhibits the progression of renal cancer cells via downregulation of the ANXA1/MAPK pathways. Moreover, we also showed that the YTHDC1/ANXA1 axis modulates the sensitivity of tyrosine kinase inhibitors. We then revealed that HDAC2 inhibitors resensitize ccRCC to tyrosine kinase inhibitors through the YY1/HDAC2 complex. We have identified a novel YY1/HDAC2/YTHDC1/ANXA1 axis modulating the progression and chemosensitivity of ccRCC. Conclusion We identified a novel YY1/HDAC2/YTHDC1/ANXA1 axis modulating the progression and chemosensitivity of ccRCC.

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“…Zhu et al. demonstrated that YTHDC1 inhibits glioma cells proliferation by decreasing VPS25 expression ( 141 ). Liu et al.…”

Section: M6a Modification and Glioblastomamentioning

confidence: 99%

The Potential Value of m6A RNA Methylation in the Development of Cancers Focus on Malignant Glioma

et al. 2022

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N6-methyladenosine (m6A) RNA methylation is an epigenetic modification that has emerged in the last few years and has received increasing attention as the most abundant internal RNA modification in eukaryotic cells. m6A modifications affect multiple aspects of RNA metabolism, and m6A methylation has been shown to play a critical role in the progression of multiple cancers through a variety of mechanisms. This review summarizes the mechanisms by which m6A RNA methylation induced peripheral cancer cell progression and its potential role in the infiltration of immune cell of the glioblastoma microenvironment and novel immunotherapy. Assessing the pattern of m6A modification in glioblastoma will contribute to improving our understanding of microenvironmental infiltration and novel immunotherapies, and help in developing immunotherapeutic strategies.

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YTHDC1-mediated VPS25 regulates cell cycle by targeting JAK-STAT signaling in human glioma cells

Cited by 28 publications

References 71 publications

Research Progress on the Regulation Mechanism of Key Signal Pathways Affecting the Prognosis of Glioma

Research Progress on the Regulation Mechanism of Key Signal Pathways Affecting the Prognosis of Glioma

YTHDC1 is downregulated by the YY1/HDAC2 complex and controls the sensitivity of ccRCC to sunitinib by targeting the ANXA1-MAPK pathway

The Potential Value of m6A RNA Methylation in the Development of Cancers Focus on Malignant Glioma

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