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. 2022 May 13;298(6):102029. doi: 10.1016/j.jbc.2022.102029

Figure 6.

Figure 6

SSTN-induced cell cycle arrest depends on activated p38MAPK.A, quantification of p38MAPK activation by antibody array (pT180/pY182) in nontransformed keratinocytes (HTE, NOK, and HaCaT) and HNSCC cells (UM-SCC47, SCC25) treated with 30 mM SSTNEGFR (left) or in-cell western of UM-SCC47 cells following treatment with SSTNEGFR, RON kinase inhibitors (BMS-777607 or CAS-913376-84-8), or ABL1 inhibitors (GNF-5 or PPY-A)(right); B, detection of pT180/pY182 p38MAPK following treatment with vehicle alone or 30 μM SSTNEGFR in nontransformed NOKs or transformed HNSCC cells; C, in nontransformed (MCF10A) or transformed (MDA-MB-231, MDA-MB-468, SKBr3) mammary epithelial cells; D, EdU-Click-IT–labeled UM-SCC47 cells treated for 3 h with either vehicle (control), 30 μM SSTNEGFR, 3 μM BMS-777607 (RON inhibitor), 0.2 μM PPY-A (ABL1 inhibitor), or 5 mM hydroxyurea (HU) in the presence or absence of 0.1 μM p38MAPK inhibitor BIRB-796 (Bar = 50 μm); E, quantification of EdU incorporation into cells treated with 30 μM SSTNEGFR with or without p38MAPK inhibitors BIRB-796 or Losmapimod for 3 h; ∗∗∗p ≤ 0.001. EdU, 5-ethynyl-2′-deoxyuridine; HNSCC, head and neck squamous cell carcinoma; HTE, human tonsillar epithelial cell; NOK, normal oral keratinocyte; P38MAPK, p38 mitogen-activated protein kinase.