TMEPAI/PMEPA1 enhances tumorigenic activities in lung cancer cells.
Bottom Line: These results suggest that constitutive expression of TMEPAI in these cancer cells depends on autocrine TGF-β stimulation.Knockdown of TMEPAI in Calu3 and NCI-H23 cells enhanced levels of Smad2 phosphorylation and significantly suppressed cell proliferation in the presence of TGF-β, indicating that highly expressed TMEPAI suppresses levels of Smad phosphorylation in these cancer cells and reduces the growth inhibitory effects of TGF-β/Smad signaling.Together, these experiments indicate that TMEPAI promotes tumorigenic activities in lung cancer cells.
Affiliation: Department of Experimental Pathology, Graduate School of Comprehensive Human Sciences and Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.Show MeSH
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Mentions: Using anti-TMEPAI (9F10) antibody, we evaluated TMEPAI expression levels in the human lung adenocarcinoma cell lines Calu3, NCI-H23, and RERF-LC-KJ. HaCaT cells were used as a positive control. HaCaT cells expressed detectable levels of TMEPAI only in the presence of more than 8 h of TGF-β stimulation; there were no detectable levels of TMEPAI without TGF-β stimulation (Fig.1a). In contrast, all three of the examined lung cancer cell lines expressed detectable levels of TMEPAI even in the absence of TGF-β stimulation. Notably, Calu3 constitutively expressed high levels of TMEPAI, whereas NCI-H23 and RERF-LC-KJ expressed distinct but relatively low levels of TMEPAI and enhanced TMEPAI expression approximately twofold in response to TGF-β (Fig.1b). Endogenous TMEPAI could also be detected as cytoplasmic dot patterns in HaCaT and NCI-H23 cells by immunofluorescence staining (Fig.1c).
Affiliation: Department of Experimental Pathology, Graduate School of Comprehensive Human Sciences and Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.