Fig. 2: FOXD1 knockdown promotes the senescence and apoptosis but inhibits the growth of HNSCC cells, whereas FOXD1 overexpression results in the opposite trend. | Cell Death Discovery

Fig. 2: FOXD1 knockdown promotes the senescence and apoptosis but inhibits the growth of HNSCC cells, whereas FOXD1 overexpression results in the opposite trend.

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. 2: FOXD1 knockdown promotes the senescence and apoptosis but inhibits the growth of HNSCC cells, whereas FOXD1 overexpression results in the opposite trend.The alternative text for this image may have been generated using AI.

A The establishment of two HNSCC cell lines with knockdown and overexpression of FOXD1 was verified at the mRNA and protein levels. The (B) EdU, (C) CCK-8, and (D) colony formation assays showed that higher FOXD1 expression levels resulted in stronger proliferation abilities. E SA-β-gal staining showed that lower FOXD1 expression levels resulted in higher proportions of senescent tumor cells. F, G Cell cycle experiments showed that FOXD1 knockdown significantly increased the G0/G1 phase ratios and reduced the S phase ratios but that FOXD1 overexpression showed the opposite trend. H, I Apoptosis experiments showed that FOXD1 knockdown increased the percentage of apoptosis cells but that FOXD1 overexpression decreased the percentage of apoptosis cells. *p < 0.05, **p < 0.01, and ***p < 0.001. FOXD1 forkhead box D1, HNSCC head and neck squamous cell carcinoma, mRNA messenger RNA, EdU 5-Ethynyl-2’-deoxyuridine, SA-β-gal senescence-associated beta-galactosidase, SEM standard error of the mean.

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