Model of methylation RBM39 by PRMT6 enhances Indisulam resistance in NSCLC.

Model of methylation RBM39 by PRMT6 enhances Indisulam resistance in NSCLC.

<p>PRMT6 methylates RBM39 at R92 in NSCLC cells. Methylation of RBM39 improves the stability of RBM39 protein via decelerating Indisulam-induced ubiquitination and proteasomal degradation. The methylated RBM39 reverses the mis-splicing of oncogenes caused by Indisulam and increases the express...

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Bibliographic Details
Main Author: Tongjia Zhang (16496661) (author)
Other Authors: Shujie Wang (750318) (author), Yue Zhou (71752) (author), Zitao Jiao (21485389) (author), Kejia Lu (7538975) (author), Xinyi Liu (186154) (author), Hui Li (32376) (author), Wei Jiang (14986) (author), Xiaowei Zhang (6505) (author)
Published: 2025
Subjects:
Biophysics
Biochemistry
Cell Biology
Genetics
Molecular Biology
Pharmacology
Biotechnology
Cancer
Hematology
Infectious Diseases
Plant Biology
Biological Sciences not elsewhere classified
xenograft mouse models
remains poorly understood
promoting alternative splicing
promotes alternative splicing
potential therapeutic strategy
binding protein 39
xlink "> indisulam
prmt6 enhances resistance
prmt6 methylates rbm39
methylation inhibits indisulam
oncogenes </ p
inhibiting prmt6
indisulam resistance
acquired resistance
ultimately leads
tumor growth
tumor efficacy
tumor activity
specific target
significantly improves
rbm39 ),
proteasomal degradation
molecular basis
malignant proliferation
line therapy
key biomarker
induced ubiquitination
closely associated
clinical efficacy
based compound
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