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. 2024 Jan 1;20(1):231–248. doi: 10.7150/ijbs.86317

Figure 5.

Figure 5

TNS4-facilitated FAK activation enhances EMT and metastasis in HNSCC cells by promoting TGFβRI and TGFβRII interaction. (A-B) Expression levels of E-cadherin, N-cadherin, and vimentin in TNS4-overexpressing cells treated with an Akt inhibitor. (C) Invasion potential of HNSCC cells under indicated treatment conditions (scale bar=200 μm). (D) The sphere-forming abilities of HNSCC cells with indicated modifications (scale bar=200 μm). (E) Western blotting analysis of p-Smad2, Smad3, p-Smad3, and Smad2 expression in HNSCC cells subjected to the indicated modifications. (F) Expression of E-cadherin, N-cadherin, vimentin, and SNAI2 in TNS4-overexpressing cells treated with LY2109761. (G-H) Effects of FAK inhibitor on the interactions between FAK and TGFβRI as well as between TGFβRI and TGFβRII. (I-J) Influence of TNS4 depletion on the interactions between FAK and TGFβRI, and between TGFβRI and TGFβRII. (K-L) Impact of TNS4 overexpression on the interactions between FAK and TGFβRI, and between TGFβRI and TGFβRII.