Fig. 5: FOXD1 regulates the proliferation ability of HNSCC by affecting activity of the p21/CDK2/Rb signaling pathway without disturbing CDK4/6. | Cell Death Discovery

Fig. 5: FOXD1 regulates the proliferation ability of HNSCC by affecting activity of the p21/CDK2/Rb signaling pathway without disturbing CDK4/6.

From: miR-30e-5p-mediated FOXD1 promotes cell proliferation by blocking cellular senescence and apoptosis through p21/CDK2/Rb signaling in head and neck carcinoma

Fig. 5: FOXD1 regulates the proliferation ability of HNSCC by affecting activity of the p21/CDK2/Rb signaling pathway without disturbing CDK4/6.The alternative text for this image may have been generated using AI.

A Western blot results showed that FOXD1 knockdown decreased the phosphorylation protein levels of CDK2 and Rb but that FOXD1 overexpression increased the phosphorylation levels of CDK2 and Rb without affecting the total protein levels. The CCK-8 assay (B, C) and colony formation assay (D, E) implied that the growth of FOXD1-overexpressing HNSCC cells was decreased after treatment with PF-07104091, a CDK2-specific inhibitor. *p < 0.05, **p < 0.01, and ***p < 0.001. FOXD1 forkhead box D1, HNSCC head and neck squamous cell carcinoma, CDK2 cyclin-dependent kinase 2, Rb retinoblastoma.

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