Figure 1 from Targeting PRMT1 Reduces Cancer Persistence and Tumor Relapse in EGFR- and KRAS-Mutant Lung Cancer
Year: 2025
Type: other
Abstract: PRMT1 is the key type I PRMT isoform mediating IFNγ/STAT1-promoted persistence. A, Effects of type I PRMT knockdown (KD) via siRNA. PC9 cells were incubated with siRNA for 2 days to ensure gene inhibition. Subsequently, cells were treated with the EGFR drug erlotinib (Erl, 2.5 μmol/L) and IFNγ (5 ng/mL) for 6 days. Cell viability was measured, and persister fitness was normalized to nontargeting control siRNA (siNTC). B, Effects of pan-type I PRMT inhibitor GSK3368715 (GSK715) with PRMT knockout (KO) cells. PC9 cells with wild-type (WT) or deleted (KO) PRMTs were cotreated with erlotinib and GSK715 (0.2 μmol/L) in the presence of IFNγ for 6 days. Persister fitness was normalized to no GSK715 (DMSO) condition for each cell line. C, Effects of PRMT1 KD via inducible shRNA. Engineered PC9 cells expressing nontargeting control shRNA (shNTC) or PRMT1-targeting shRNA (siPRMT1 #1 and #2) were treated with the EGFR drug osimertinib (Osi, 100 nmol/L) in the presence of IFNγ for 6 days. Doxycycline (Dox, 100 ng/mL) was administered concurrently to induce PRMT1 knockdown. Persister fitness was normalized to the no Dox condition for each cell line. All data are reported as mean ± standard deviation, with three to five replicates per condition. Statistical comparisons between groups were based on unpaired, two-sided Student t tests. The significance of the results is indicated by symbols: not significant (ns), P > 0.05; *, P ≤ 0.05; ***, P ≤ 0.001; ****, P ≤ 0.0001.
Language: English
Subfield: Pulmonary and Respiratory Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: gold
OpenAlex ID: W4406630787