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. Author manuscript; available in PMC: 2025 Jun 3.
Published in final edited form as: Mol Cancer Ther. 2024 Dec 3;23(12):1801–1814. doi: 10.1158/1535-7163.MCT-24-0369

Figure 5. CDK4/6 and MEK inhibition triggers transposable element upregulation in lung and PDAC models.

Figure 5.

A. Volcano plot displaying differentially expressed transposable elements in combined CDK4/6i (Palbociclib, 100 nM) and MEKi (Trametinib, 25 nM)-treated compared to DMSO-treated 519 and 3226 cell lines. B. Transposable element analysis using TEtranscripts to analyze the differential expression of transposable elements in different PDAC and lung cancer cell lines treated with CDK4/6i (Palbociclib, 0.5 μM) and MEKi (Trametinib, 25 nM) in combination. C. Venn diagram showing distribution of significantly upregulated transposable elements in different lung and PDAC cell models treated with CDK4/6i (Palbociclib, 0.5 μM) and MEKi (Trametinib, 25 nM) in combination. D. Heatmap displaying log fold change of the 6 conserved upregulated transposable elements from the five indicated cell lines treated with CDK4/6i (Palbociclib, 100 nM for 519 and 3226 cells; 0.5 μM for PA-TU 8988T, MIA PaCa-2 and A549 cells) and MEKi (Trametinib, 25 nM) in combination. E. qPCR analysis of ERV3–1 expression in CDK4/6i (Palbociclib, 100 nM) and MEKi (Trametinib, 25 nM)-treated 3226 and 519 cells over 48 h post-treatment. Data displayed as mean ± SD in triplicate. * p < 0.05, **** p < 0.0001 as determined by students t test with multiple comparisons. TE, transposable element.