Proteomics

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Protein arginine methyltransferase 5 (PRMT5) is an actionable therapeutic target in CDK4/6 inhibitor-resistant ER+/RB-deficient breast cancer

ABSTRACT: PRMT5 Co-IP mass spectrometry: Lysates of MCF-7 RB1-knockout cells were pulled down with a PRMT5 antibody or IgG control. The pulldowns were subjected to mass spectrometry analysis. QEX2_981005, QEX2_981006, QEX2_981007: DMSO, IgG QEX2_981008, QEX2_981009, QEX2_981010: DMSO, PRMT5 antibody QEX2_981011, QEX2_981012, QEX2_981013, GSK, IgG QEX2_981014, QEX2_981015, QEX2_981016, GSK, PRMT5 antibody SDMA PTM analysis: MCF-7 RB1-knockout cells were transfected with a PRMT5 siRNA or a control siRNA. Lysates were collected three days after transfection and subjected to mass spectrometry analysis. LUM1_1000791, LUM1_1000792, LUM1_1000793: control SiRNA LUM1_1000794, LUM1_1000795, LUM1_1000796: PRMT5 siRNA [

INSTRUMENT(S): Orbitrap Fusion Lumos, Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture

SUBMITTER: Joe Otto  

LAB HEAD: Carlos L. Arteaga

PROVIDER: PXD046996 | Pride | 2024-01-12

REPOSITORIES: Pride

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Dataset's files

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Action DRS
IP.msf Msf
LUM1_1000791.mgf Mgf
LUM1_1000791.raw Raw
LUM1_1000792.mgf Mgf
LUM1_1000792.raw Raw
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Publications

CDK4/6 inhibitors (CDK4/6i) have improved survival of patients with estrogen receptor-positive (ER+) breast cancer. However, patients treated with CDK4/6i eventually develop drug resistance and progress. <i>RB1</i> loss-of-function alterations confer acquired resistance to CDK4/6i, but the optimal therapy for these patients is unclear. Using a genome-wide CRISPR screen, we identified protein arginine methyltransferase 5 (PRMT5) as a molecular vulnerability in ER+/<i>RB1</i>-knockout (RBKO) breas  ...[more]

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