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Epigenetic reader ZMYND11 noncanonical function restricts HNRNPA1-mediated stress granule formation and oncogenic activity

ABSTRACT: Epigenetic reader ZMYND11 noncanonical function restricts HNRNPA1-mediated stress granule formation and oncogenic activity, PPI of ZMYND11 in LNCap

ORGANISM(S): Homo Sapiens

SUBMITTER: Gonghong Wei

PROVIDER: PXD055421 | iProX | Wed Aug 28 00:00:00 BST 2024

REPOSITORIES: iProX

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Epigenetic reader ZMYND11 noncanonical function restricts HNRNPA1-mediated stress granule formation and oncogenic activity.

Lian Cheng C Zhang Chunyi C Tian Pan P Tan Qilong Q Wei Yu Y Wang Zixian Z Zhang Qin Q Zhang Qixiang Q Zhong Mengjie M Zhou Li-Quan LQ Ke Xisong X Zhang Huabing H Zhu Yao Y Li Zhenfei Z Cheng Jingdong J Wei Gong-Hong GH

Signal transduction and targeted therapy 20240928 1

Epigenetic readers frequently affect gene regulation, correlate with disease prognosis, and hold significant potential as therapeutic targets for cancer. Zinc finger MYND-type containing 11 (ZMYND11) is notably recognized for reading the epigenetic marker H3.3K36me3; however, its broader functions and mechanisms of action in cancer remain underexplored. Here, we report that ZMYND11 downregulation is prevalent across various cancers and profoundly correlates with poorer outcomes in prostate cance ...[more]

PMID: 39341825

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Epigenetic reader ZMYND11 noncanonical function restricts HNRNPA1-mediated stress granule formation and oncogenic activity

Project description:Epigenetic reader ZMYND11 noncanonical function restricts HNRNPA1-mediated stress granule formation and oncogenic activity, To investigate the function of ZMYND11 in prostate cancer, We performed Co-IP and mass-spectometry (MS) analysis of ZMYND11.

2024-08-27 | PXD055219 |

Epigenetic reader ZMYND11 noncanonical function restricts HNRNPA1-mediated stress granule formation and oncogenic activity

Project description:Epigenetic reader ZMYND11 noncanonical function restricts HNRNPA1-mediated stress granule formation and oncogenic activity

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Epigenetic reader ZMYND11 noncanonical function restricts HNRNPA1-mediated stress granule formation and oncogenic activity.

Project description:Epigenetic readers frequently affect gene regulation, correlate with disease prognosis, and hold significant potential as therapeutic targets for cancer. Zinc finger MYND-type containing 11 (ZMYND11) is notably recognized for reading the epigenetic marker H3.3K36me3; however, its broader functions and mechanisms of action in cancer remain underexplored. Here, we report that ZMYND11 downregulation is prevalent across various cancers and profoundly correlates with poorer outcomes in prostate cancer patients. Depletion of ZMYND11 promotes tumor cell growth, migration, and invasion in vitro, as well as tumor formation and metastasis in vivo. Mechanistically, we discover that ZMYND11 exhibits tumor suppressive roles by recognizing arginine-194-methylated HNRNPA1 dependent on its MYND domain, thereby retaining HNRNPA1 in the nucleus and preventing the formation of stress granules in the cytoplasm. Furthermore, ZMYND11 counteracts the HNRNPA1-driven increase in the PKM2/PKM1 ratio, thus mitigating the aggressive tumor phenotype promoted by PKM2. Remarkably, ZMYND11 recognition of HNRNPA1 can be disrupted by pharmaceutical inhibition of the arginine methyltransferase PRMT5. Tumors with low ZMYND11 expression show sensitivity to PRMT5 inhibitors. Taken together, our findings uncover a previously unexplored noncanonical role of ZMYND11 as a nonhistone methylation reader and underscore the critical importance of arginine methylation in the ZMYND11-HNRNPA1 interaction for restraining tumor progression, thereby proposing novel therapeutic targets and potential biomarkers for cancer treatment.

| S-EPMC11438962 | biostudies-literature

Epigenetic reader ZMYND11 noncanonical function restricts HNRNPA1-mediated stress granule formation and oncogenic activity

Project description:To investigate the function of ZMYND11 in prostate cancer, we knockdown ZMYND11 in 22Rv1 cells and do RNA-seq.

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The methylarginine reader function of SND1 is oncogenic

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Transcription profiling of mouse with Hedgehog-induced medulloblastoma reveals oncogenic Hedgehog signaling promotes medulloblastoma from lineage-restricted granule cell progenitors

Project description:Origins of the brain tumor, medulloblastoma, from stem cells or restricted pro-genitor cells are unclear. To investigate this, we activated oncogenic Hedgehog signaling in multipotent and lineage-restricted CNS progenitors. We observed that normal unipo-tent cerebellar granule neuron precursors (CGNP) derive from hGFAP+ and Olig2+ rhombic lip progenitors. Hedgehog activation in a spectrum of early and late stage CNS progenitors generated similar medulloblastomas, but not other brain cancers, indicating that acquisition of CGNP identity is essential for tumorigenesis. We show in human and mouse medulloblastoma that cells expressing the glia-associated markers Gfap and Olig2 are neoplastic and that they retain features of embryonic-type granule lineage progenitors. Thus, oncogenic Hedgehog signaling promotes medulloblastoma from lineage-restricted granule cell progenitors. Gene expression profiling of cerebellar tumors generated from various early and late stage CNS progenitor cells. Experiment Overall Design: Group comparisons with biological replicates

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Lineage-specific intolerance to oncogenic drivers restricts histological transformation

Project description:Lineage-specific intolerance to oncogenic drivers restricts histological transformation

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Lineage-specific intolerance to oncogenic drivers restricts histological transformation [scRNA-Seq]

Project description:Lineage-specific intolerance to oncogenic drivers restricts histological transformation [scRNA-Seq]

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Lineage-specific intolerance to oncogenic drivers restricts histological transformation [ATAC-Seq]

Project description:Lineage-specific intolerance to oncogenic drivers restricts histological transformation [ATAC-Seq]

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The histone acetylation reader ENL is required for oncogenic transcription driven by super-enhancer and represents a synergistic vulnerability for BET inhibition [RNA-seq]

Project description:The histone acetylation reader ENL is identifed as a key factor controlling super-enhancer-driven transcription. Therefore, we constructed a targeted degradation system of endogenous ENL protein and investigated the roles of ENL in regulating oncogenic transcription through epigenetic reprogramming.

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