PRMT1 potentiates chondrosarcoma development through activation of YAP activity

Chen, Changbao; Zhou, Hua; Zhang, Xiaolin; Liu, Zhongjun; Ma, Xiaofang

doi:10.1002/mc.23108

Cited by 14 publications

(20 citation statements)

References 41 publications

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“…Although YAP/TAZ were not investigated in these studies, it may be speculated that the observed molecular alterations affected chondrosarcoma adherence and invasion phenotypes through abrogated YAP/TAZ signaling. A recent study identified YAP nuclear accumulation as a consequence of LATS1 inactivation by protein arginine methyltransferase 1 (PRMT1) as an independent bad prognostic factor in chondrosarcoma [181]. Finally, the treatment of chondrosarcoma cells with the BET-bromodomain inhibitor JQ1 downregulated YAP/TAZ and LATS1, leading to the upregulation of cyclin-dependent kinase inhibitor 1a (CDKN1A/p21) and cell cycle arrest, senescence and apoptosis [182].…”

Section: Yap/taz In Chondrosarcomamentioning

confidence: 99%

The YAP/TAZ Pathway in Osteogenesis and Bone Sarcoma Pathogenesis

Kovar

Bierbaumer

Radic-Sarikas

2020

Cells

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YAP and TAZ are intracellular messengers communicating multiple interacting extracellular biophysical and biochemical cues to the transcription apparatus in the nucleus and back to the cell/tissue microenvironment interface through the regulation of cytoskeletal and extracellular matrix components. Their activity is negatively and positively controlled by multiple phosphorylation events. Phenotypically, they serve an important role in cellular plasticity and lineage determination during development. As they regulate self-renewal, proliferation, migration, invasion and differentiation of stem cells, perturbed expression of YAP/TAZ signaling components play important roles in tumorigenesis and metastasis. Despite their high structural similarity, YAP and TAZ are functionally not identical and may play distinct cell type and differentiation stage-specific roles mediated by a diversity of downstream effectors and upstream regulatory molecules. However, YAP and TAZ are frequently looked at as functionally redundant and are not sufficiently discriminated in the scientific literature. As the extracellular matrix composition and mechanosignaling are of particular relevance in bone formation during embryogenesis, post-natal bone elongation and bone regeneration, YAP/TAZ are believed to have critical functions in these processes. Depending on the differentiation stage of mesenchymal stem cells during endochondral bone development, YAP and TAZ serve distinct roles, which are also reflected in bone tumors arising from the mesenchymal lineage at different developmental stages. Efforts to clinically translate the wealth of available knowledge of the pathway for cancer diagnostic and therapeutic purposes focus mainly on YAP and TAZ expression and their role as transcriptional co-activators of TEAD transcription factors but rarely consider the expression and activity of pathway modulatory components and other transcriptional partners of YAP and TAZ. As there is a growing body of evidence for YAP and TAZ as potential therapeutic targets in several cancers, we here interrogate the applicability of this concept to bone tumors. To this end, this review aims to summarize our current knowledge of YAP and TAZ in cell plasticity, normal bone development and bone cancer.Cells 2020, 9, 972 2 of 34 co-activators Yes-associated protein 1 (YAP-1, YAP) and its paralogue, the transcriptional co-activator with PDZ-binding motif (TAZ, WWTR1), which are typically controlled on the post-translational level by upstream regulatory signaling pathways in organ development and tissue homeostasis [2,3]. YAP and TAZ were reported to affect self-renewal and lineage commitment of stem cells [4][5][6][7], while hyperactivation of YAP and TAZ have been linked to cancer growth and metastasis in various tumors [8][9][10]. TAZ levels are elevated in approximately 20% of cancers and drive invasion and metastasis [11,12], while YAP is frequently overexpressed or amplified in cancer and was shown to promote resistance to chemotherapy in oncogene-addicted tumors up...

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Section: Yap/taz In Chondrosarcomamentioning

confidence: 99%

The YAP/TAZ Pathway in Osteogenesis and Bone Sarcoma Pathogenesis

Kovar

Bierbaumer

Radic-Sarikas

2020

Cells

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“… 19 Clinical clinicopathological information and follow-up data were reported previously, and signed informed consent for sample collection and analysis were obtained from all patients and was in full compliance with national legislation and the ethical standards as described previously (IRB00001052-08044). 20 , 21 Human chondrosarcoma SW1353 cell line was purchased from the American Type Culture Collection (Bethesda, MD, USA) and maintained in Dulbecco’s modified Eagle medium (DMEM, Gibco, Grand Island, NY, USA) containing 10% fetal bovine serum (FBS, Gibco) and cultured in a humidified cell incubator with 5% CO 2 at 37°C.…”

Section: Methodsmentioning

confidence: 99%

“…Detailed experimental protocols have been described previously. 19 , 20 Typically, after antigen retrieval, ZNF395 (Proteintech, 13149-1-AP; 1:100) immunoreactivities were detected using the EnVision+, Peroxidase system (DAKO Diagnostics, Denmark). The slides were incubated with DAB substrate (DAKO Diagnostics, Denmark) and counterstained with hematoxylin.…”

Section: Methodsmentioning

confidence: 99%

“…Cell Counting Kit-8 (Dojindo, Kumamoto, Japan) for cell viability, and clonogenic formation assays were conducted as described previously. 20 , 23 Briefly, SW1353 cells were seeded into 96-well plates at 5000 cells per well for 24 hours and assessed using CCK-8 at the indicated time. For clonogenic assay, after treatment, the number of viable cell colonies was determined after either 10 days SW1353 cells post inoculation of 150 cells per well in triplicate in 12-well plates.…”

Section: Methodsmentioning

confidence: 99%

“…Colonies were counted after methanol/acetone (1:1) fixation and Gentian Violet staining according to the previous experimental protocols. 20 …”

Section: Methodsmentioning

confidence: 99%

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Dysregulation of Zinc Finger Protein 395 Contributes to the Pathogenesis of Chondrosarcoma

Chen¹,

Zhou²,

Liu³

et al. 2021

OTT

Self Cite

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Introduction The transcription factor zinc finger protein 395 (ZNF395) is involved in several cellular responses and tumorigenesis. However, the potential role and clinical significance of ZNF395 in chondrosarcoma are not well investigated. This study determines the expression profile, prognostic value and biological function of ZNF395 in human chondrosarcoma. Methods The mRNA and protein expressions of ZNF395 in fresh chondrosarcomas and the matched adjacent non-tumor tissues were assessed using real-time PCR and immunoblotting, respectively. The protein expression of ZNF395 in chondrosarcoma specimens was evaluated by immunohistochemistry, and the relationships among its protein level, clinicopathological parameters and prognosis were further detected. Cell viability, colony formation, migration, invasion and apoptosis assay were evaluated in chondrosarcoma cells with depletion of ZNF395. Results The mRNA and protein expressions of ZNF395 in chondrosarcoma tissues were significantly higher than those in the matched adjacent non-tumor tissues and benign cartilage tumors. Clinical analysis displayed that ZNF395 was expressed at higher levels in chondrosarcoma patients with higher histological grade and advanced MSTS stage. Furthermore, we demonstrated that high expression of ZNF395 correlated with a worse overall survival of chondrosarcoma patients. Multivariate Cox regression analysis indicated that ZNF395 was an independent prognostic marker in chondrosarcoma patients. Functional studies revealed that depletion of ZNF395 markedly inhibited cell viability, colony formation, migration and invasion, and promoted apoptosis in chondrosarcoma. Conclusion These findings suggest that dysregulation of ZNF395 contributes to chondrosarcoma development, and ZNF395 may act as a potent oncogene and serve as a independently prognostic factor, highlight the potential of ZNF395 as a novel biomarker and therapeutic target for chondrosarcoma.

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PRMT1‐mediated arginine methylation promotes YAP activation and hepatocellular carcinoma proliferation

Yu,

Peng

et al. 2024

FEBS Open Bio

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The activity of Hippo signaling is commonly dysregulated in various human malignancies, including hepatocellular carcinoma (HCC). YAP, the key effector of Hippo pathway, is regulated through several posttranslational modifications. However, the mechanism by which YAP is regulated by arginine methylation remains unknown. In this study, immunoprecipitation and mass spectrometry were used to identify the arginine methylation site of YAP in HCC cells. The transcriptional activity of YAP and TEAD were further characterized by real‐time qPCR and immunofluorescence assay, and a subcutaneous and orthotopic tumor mouse model was used to assess the effect of PRMT1‐knockdown on HCC tumor growth. The result of mass spectrometry analysis identified that YAP was methylated at arginine 124. Moreover, we found that arginine methyltransferase PRMT1 interacted with YAP to mediate its arginine methylation, thus inhibited YAP phosphorylation and promoted YAP activity in the nucleus. PRMT1 was up‐regulated in HCC tissues and positively associated with the expressions of YAP target genes. Silencing PRMT1 in HCC cells inhibited cell proliferation and tumor growth, while PRMT1‐overexpression promoted HCC growth through YAP methylation. Our study reveals that PRMT1‐mediated arginine methylation at R124 is mutually exclusive with YAP S127 phosphorylation, thereby facilitating YAP activity in the nucleus and promoting tumorigenesis in HCC.

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PRMT1 potentiates chondrosarcoma development through activation of YAP activity

Cited by 14 publications

References 41 publications

The YAP/TAZ Pathway in Osteogenesis and Bone Sarcoma Pathogenesis

The YAP/TAZ Pathway in Osteogenesis and Bone Sarcoma Pathogenesis

Dysregulation of Zinc Finger Protein 395 Contributes to the Pathogenesis of Chondrosarcoma

PRMT1‐mediated arginine methylation promotes YAP activation and hepatocellular carcinoma proliferation

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