Fig. 6: Effect of CSNK1D knockdown on the orthotopic head and neck tumor growth in vivo. | Cell Death & Disease

Fig. 6: Effect of CSNK1D knockdown on the orthotopic head and neck tumor growth in vivo.

From: CSNK1D inhibition suppresses head and neck squamous cell carcinoma progression through SHH and PTCH1 pathway

Fig. 6: Effect of CSNK1D knockdown on the orthotopic head and neck tumor growth in vivo.

a Schematic diagram of the subcutaneous implantation of HNSCC cell lines in nude mice. b Evaluation of mouse body weights every four days for two weeks after tumor cell injection. c Tumor images of the HN4-NC and HN4-sh-CSNK1D cells in subcutaneous tissues. d Sizes of tumors in the HN4-NC and HN4-sh-CSNK1D cells in subcutaneous tissues at the end of the experiment. e Protein expression of CSNK1D, N-cadherin, E-cadherin, vimentin, Bax, and Bcl2 in mouse orthotopic tumor tissues. f Representative IHC staining images of CSNK1D, ki67 and BCL2 in mouse orthotopic tumor tissues (scale bar, 100 μm). g Venn diagram demonstrating the overlapping of the drugs targeting CSNK1D predicted by DGIDB and L1000FWB. h List of binding affinity of CSNK1D and predicted drugs, Pattern diagram of the combination of CSNK1D and drug SB-203580. i Co-ip between CSNK1D, shh and ptch1 in HN4 and CAL27 cells treated with SB-203580. j Schematic diagram of orthotopic tumor model treated with PBS or SB-203580. k Representative images of tumors from orthotopic tumor model treated with phosphate-buffered saline (PBS) or SB-203580. l Sizes of tumors in the HN4 cells treated with PBS or SB-203580 in subcutaneous tissues at the end of the experiment. m Representative IHC staining images of BCL2, BAX and KI67 in orthotopic tumor tissues treated with PBS or SB-203580 (scale bar, 100 μm). n Schematic illustration showing the suggested mechanism by which CSNK1D functions as an oncogene for HNSCC apoptosis through the hedgehog pathway. CSNK1D contributes to stable SHH and PTCH1 complexes to promote the nucleus entry of GLI1 to regulate BCL2 transcription.

Back to article page