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The team led by Tang Hailin from Sun Yat-sen University Cancer Center discovered that protein arginine methyltransferase 1 (PRMT1) activates downstream signaling pathways by methylating PARP1, thereby driving lung metastasis and chemotherapy resistance in triple-negative breast cancer. The related findings were published in Research under the title "PRMT1-Mediated PARP1 Methylation Drives Lung Metastasis and Chemoresistance via P65 Activation in Triple-Negative Breast Cancer". Citation: Zhang J, Huang Z, Song C, Wu S, Xie J, Zou Y, Xie X, Wu T, Yang H, Tang H. PRMT1-Mediated PARP1 Methylation Drives Lung Metastasis and Chemoresistance via P65 Activation in Triple-Negative Breast Cancer. Research. 2025 Sep 8; 8: 0854.
https://doi.org/10.34133/research.0854.
I. Research Background
Triple-negative breast cancer (TNBC) is the most aggressive subtype of breast cancer, characterized by high metastatic tendency, poor prognosis, and limited treatment options. The global incidence of breast cancer is continuously increasing, and some patients experience distant metastasis after diagnosis, with the lung being the most common site of metastasis for breast cancer. Currently, chemotherapy remains the main treatment for TNBC, but the emergence of chemotherapy resistance significantly affects treatment outcomes, resulting in poor prognosis for patients. Therefore, in-depth analysis of the molecular mechanisms underlying TNBC lung metastasis and chemotherapy resistance, as well as the exploration of potential therapeutic targets, is of great significance for improving the clinical prognosis of patients.
PRMT1, as a key protein arginine methyltransferase, participates in the regulation of protein stability, cell signal transduction, and other biological processes. Studies have shown that it is related to the proliferation and metastasis of TNBC. However, the specific role and mechanism of PRMT1 in lung metastasis and chemotherapy resistance remain unclear. This study clarifies that PRMT1 methylates PARP1 to activate the NF-κB signaling pathway, simultaneously enhancing the characteristics of tumor stem cells and inhibiting anti-tumor immunity, ultimately promoting TNBC lung metastasis and chemotherapy resistance, providing new targets and strategies for the precise treatment of TNBC.
