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TMEPAI/PMEPA1 enhances tumorigenic activities in lung cancer cells.

Vo Nguyen TT, Watanabe Y, Shiba A, Noguchi M, Itoh S, Kato M - Cancer Sci. (2014)

Bottom Line: TMEPAI is constitutively and highly expressed in many types of cancer and is associated with poor prognosis.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Experimental Pathology, Graduate School of Comprehensive Human Sciences and Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.

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Enhanced expression of TMEPAI in lung cancer cells. (a) Induction of TMEPAI by 5 ng/mL transforming growth factor-β (TGF-β) in HaCaT cells. Endogenous TMEPAI was detected by a monoclonal anti-TMEPAI antibody (9F10). β-actin was used as the loading control. Relative amounts of TMEPAI (TMEPAI/β-actin) were measured by NIH Image and are shown below the panel. (b) Expression of TMEPAI in the lung cancer cell lines Calu3, RERF-LC-KJ, and NCI-H23 detected as in (a). (c) HaCaT or NCI-B23 cells were treated with 5 ng/mL TGF-β as indicated. After treatment, the cells were subjected to fluorescence microscopy using anti-TMEPAI antibody.
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fig01: Enhanced expression of TMEPAI in lung cancer cells. (a) Induction of TMEPAI by 5 ng/mL transforming growth factor-β (TGF-β) in HaCaT cells. Endogenous TMEPAI was detected by a monoclonal anti-TMEPAI antibody (9F10). β-actin was used as the loading control. Relative amounts of TMEPAI (TMEPAI/β-actin) were measured by NIH Image and are shown below the panel. (b) Expression of TMEPAI in the lung cancer cell lines Calu3, RERF-LC-KJ, and NCI-H23 detected as in (a). (c) HaCaT or NCI-B23 cells were treated with 5 ng/mL TGF-β as indicated. After treatment, the cells were subjected to fluorescence microscopy using anti-TMEPAI antibody.

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).


TMEPAI/PMEPA1 enhances tumorigenic activities in lung cancer cells.

Vo Nguyen TT, Watanabe Y, Shiba A, Noguchi M, Itoh S, Kato M - Cancer Sci. (2014)

Enhanced expression of TMEPAI in lung cancer cells. (a) Induction of TMEPAI by 5 ng/mL transforming growth factor-β (TGF-β) in HaCaT cells. Endogenous TMEPAI was detected by a monoclonal anti-TMEPAI antibody (9F10). β-actin was used as the loading control. Relative amounts of TMEPAI (TMEPAI/β-actin) were measured by NIH Image and are shown below the panel. (b) Expression of TMEPAI in the lung cancer cell lines Calu3, RERF-LC-KJ, and NCI-H23 detected as in (a). (c) HaCaT or NCI-B23 cells were treated with 5 ng/mL TGF-β as indicated. After treatment, the cells were subjected to fluorescence microscopy using anti-TMEPAI antibody.
© Copyright Policy - open-access
Related In: Results  -  Collection

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fig01: Enhanced expression of TMEPAI in lung cancer cells. (a) Induction of TMEPAI by 5 ng/mL transforming growth factor-β (TGF-β) in HaCaT cells. Endogenous TMEPAI was detected by a monoclonal anti-TMEPAI antibody (9F10). β-actin was used as the loading control. Relative amounts of TMEPAI (TMEPAI/β-actin) were measured by NIH Image and are shown below the panel. (b) Expression of TMEPAI in the lung cancer cell lines Calu3, RERF-LC-KJ, and NCI-H23 detected as in (a). (c) HaCaT or NCI-B23 cells were treated with 5 ng/mL TGF-β as indicated. After treatment, the cells were subjected to fluorescence microscopy using anti-TMEPAI antibody.
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).

Bottom Line: TMEPAI is constitutively and highly expressed in many types of cancer and is associated with poor prognosis.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Experimental Pathology, Graduate School of Comprehensive Human Sciences and Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.

Show MeSH
Related in: MedlinePlus