PRMT1 Regulates EGFR and Wnt Signaling Pathways and Is a Promising Target for Combinatorial Treatment of Breast Cancer

Suresh, Samyuktha; Huard, S.; Brisson, Amélie; Némati, Fariba; Dakroub, Rayan; Poulard, Coralie; Ye, Mengliang; Martel, Elise; Réyès, Cécile; Silvestre, David C.; Meseure, Didier; André, Nathalie; Gentien, David; Fayyad‐Kazan, Hussein; Romancer, Muriel Le; Decaudin, Didier; Roman‐Roman, Sergio; Dubois, Thierry

doi:10.3390/cancers14020306

Cited by 23 publications

(20 citation statements)

References 67 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Recent cancer-related studies on the role of PRMTs are summarized in Table III. In TNBC, PRMT1 regulates the EGFR and the Wnt signalling pathways (80). Type I PRMT inhibitors decrease breast cancer cell proliferation and have anti-tumour activity.…”

Section: Methylation Of Nonhistonesmentioning

confidence: 99%

Research progress on PRMTs involved in epigenetic modification and tumour signalling pathway regulation (Review)

Niu

Liu

et al. 2023

Int J Oncol

View full text Add to dashboard Cite

Posttranslational modification (PTM) of proteins is essential for increasing protein diversity and maintaining cellular homeostasis, but uncontrolled modification may lead to tumorigenesis. Arginine methylation is a tumorigenesis-related PTM that affects protein function through protein-protein and protein-nucleic acid interactions. Protein arginine methyltransferases (PRMTs) have vital roles in signalling pathways of tumour-intrinsic and tumour-extrinsic microenvironments. The present review summarizes the modifications and functions of PRMTs in histone methylation and nonhistone methylation, their roles in RNA splicing and DNA damage repair and the currently known functions in tumour metabolism and immunotherapy. In conclusion, this article reviews the latest research progress on the role of PRMTs in tumour signal transduction, providing a theoretical basis for clinical diagnosis and treatment. Targeting PRMTs is expected to provide new directions for tumour therapy.

show abstract

Section: Methylation Of Nonhistonesmentioning

confidence: 99%

Research progress on PRMTs involved in epigenetic modification and tumour signalling pathway regulation (Review)

Niu

Liu

et al. 2023

Int J Oncol

View full text Add to dashboard Cite

show abstract

“…Studies have demonstrated that PRMT1 expression is upregulated in TNBC and contributes to tumor progression and chemotherapy resistance. [ 20 ] Metabric and TCGA databases also indicated that PRMT1 expression is upregulated in breast cancer, especially in TNBC (Figure S4A–C, Supporting Information). We then performed clone formation and MTT assays in TNBC cells before hypoxic treatment and found that the overexpression of PRMT1 could diminish the inhibition of cancer cell proliferation by downregulating circTBC1D14 expression (Figure S4D,E, Supporting Information).…”

Section: Resultsmentioning

confidence: 99%

Hypoxia‐Induced FUS–circTBC1D14 Stress Granules Promote Autophagy in TNBC

Liu

et al. 2023

Advanced Science

View full text Add to dashboard Cite

Triple‐negative breast cancer (TNBC) is a highly aggressive subtype of breast cancer that is suggested to be associated with hypoxia. This study is the first to identify a novel circular RNA (circRNA), circTBC1D14, whose expression is significantly upregulated in TNBC. The authors confirm that high circTBC1D14 expression is associated with a poor prognosis in patients with breast cancer. circTBC1D14‐associated mass spectrometry and RNA‐binding protein‐related bioinformatics strategies indicate that FUS can interact with circTBC1D14, which can bind to the downstream flanking sequence of circTBC1D14 to induce cyclization. FUS is an essential biomarker associated with stress granules (SGs), and the authors find that hypoxic conditions can induce FUS–circTBC1D14‐associated SG formation in the cytoplasm after modification by protein PRMT1. Subsequently, circTBC1D14 increases the stability of PRMT1 by inhibiting its K48‐regulated polyubiquitination, leading to the upregulation of PRMT1 expression. In addition, FUS–circTBC1D14 SGs can initiate a cascade of SG‐linked proteins to recognize and control the elimination of SGs by recruiting LAMP1 and enhancing lysosome‐associated autophagy flux, thus contributing to the maintenance of cellular homeostasis and promoting tumor progression in TNBC. Overall, these findings reveal that circTBC1D14 is a potential prognostic indicator that can serve as a therapeutic target for TNBC treatment.

show abstract

“…Our study demonstrate that PRMT1 suppresses colon cancer, which can provide a more comprehensive knowledge of the underlying mechanisms of PRMT1 in cancer progression. PRMT1 has been known as an oncogene via stimulating cancer cell proliferation or blocking apoptosis [ 36 , 39 ], while the opposite findings have also been reported in some experiments in which PRMT1 might inhibit proliferation and promote apoptosis in cancer [ 37 , 38 ]. Despite of regulating cancer cell proliferation and apoptosis, we provide another mechanism driven by PRMT1, in which PRMT1 inhibits necroptotic cell death.…”

Section: Discussionmentioning

confidence: 99%

PRMT1 reverts the immune escape of necroptotic colon cancer through RIP3 methylation

Jiang

et al. 2023

Cell Death Dis

View full text Add to dashboard Cite

Necroptosis plays a double-edged sword role in necroptotic cancer cell death and tumor immune escape. How cancer orchestrates necroptosis with immune escape and tumor progression remains largely unclear. We found that RIP3, the central activator of necroptosis, was methylated by PRMT1 methyltransferase at the amino acid of RIP3 R486 in human and the conserved amino acid R479 in mouse. The methylation of RIP3 by PRMT1 inhibited the interaction of RIP3 with RIP1 to suppress RIP1-RIP3 necrosome complex, thereby blocking RIP3 phosphorylation and necroptosis activation. Moreover, the methylation-deficiency RIP3 mutant promoted necroptosis, immune escape and colon cancer progression due to increasing tumor infiltrated myeloid-derived immune suppressor cells (MDSC), while PRMT1 reverted the immune escape of RIP3 necroptotic colon cancer. Importantly, we generated a RIP3 R486 di-methylation specific antibody (RIP3ADMA). Clinical patient samples analysis revealed that the protein levels of PRMT1 and RIP3ADMA were positively correlated in cancer tissues and both of them predicted the longer patient survival. Our study provides insights into the molecular mechanism of PRMT1-mediated RIP3 methylation in the regulation of necroptosis and colon cancer immunity, as well as reveals PRMT1 and RIP3ADMA as the valuable prognosis markers of colon cancer.

show abstract

PRMT1 Regulates EGFR and Wnt Signaling Pathways and Is a Promising Target for Combinatorial Treatment of Breast Cancer

Cited by 23 publications

References 67 publications

Research progress on PRMTs involved in epigenetic modification and tumour signalling pathway regulation (Review)

Research progress on PRMTs involved in epigenetic modification and tumour signalling pathway regulation (Review)

Hypoxia‐Induced FUS–circTBC1D14 Stress Granules Promote Autophagy in TNBC

PRMT1 reverts the immune escape of necroptotic colon cancer through RIP3 methylation

Contact Info

Product

Resources

About