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Erschienen in: Tumor Biology 12/2015

01.12.2015 | Research Article

TGIF1 promoted the growth and migration of cancer cells in nonsmall cell lung cancer

verfasst von: Guo Xiang, Yang Yi, He Weiwei, Wu Weiming

Erschienen in: Tumor Biology | Ausgabe 12/2015

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Abstract

Transforming growth factor beta-inducing factor 1 (TGIF1) was reported to be dysregulated in several types of cancer. However, its expression pattern and functions in nonsmall cell lung cancer (NSCLC) remained unknown. In the present study, the expression of TGIF1 was found to be elevated in the clinical NSCLC tissues. TGIF1 promoted the growth and migration of NSCLC cells, while knocking down the expression of TGIF1 inhibited the growth and migration of NSCLC cells. Moreover, downregulation of TGIF1 impaired the metastasis of NSCLC cells. In the study for the molecular mechanisms, it was found that TGIF1 positively regulated beta-catenin/TCF signaling. In summary, our study demonstrated the oncogenic role of TGIF1 in NSCLC, and TGIF1 might be a therapeutic target for NSCLC.
Literatur
1.
Zurück zum Zitat DeSantis CE, Lin CC, Mariotto AB, et al. Cancer treatment and survivorship statistics, 2014. CA Cancer J Clin. 2014;64(4):252–71.CrossRefPubMed DeSantis CE, Lin CC, Mariotto AB, et al. Cancer treatment and survivorship statistics, 2014. CA Cancer J Clin. 2014;64(4):252–71.CrossRefPubMed
2.
Zurück zum Zitat Siegel R, Ma J, Zou Z, Jemal A. Cancer statistics, 2014. CA Cancer J Clin. 2014;64(1):9–29.CrossRefPubMed Siegel R, Ma J, Zou Z, Jemal A. Cancer statistics, 2014. CA Cancer J Clin. 2014;64(1):9–29.CrossRefPubMed
3.
Zurück zum Zitat Lee CK, Brown C, Gralla RJ, et al. Impact of EGFR inhibitor in non-small cell lung cancer on progression-free and overall survival: a meta-analysis. J Natl Cancer Inst. 2012;105(9):595–605.CrossRef Lee CK, Brown C, Gralla RJ, et al. Impact of EGFR inhibitor in non-small cell lung cancer on progression-free and overall survival: a meta-analysis. J Natl Cancer Inst. 2012;105(9):595–605.CrossRef
4.
Zurück zum Zitat Oxnard GR, Janjigian YY, Arcila ME, et al. Maintained sensitivity to EGFR tyrosine kinase inhibitors in EGFR-mutant lung cancer recurring after adjuvant erlotinib or gefitinib. Clin Cancer Res. 2012;17(19):6322–8.CrossRef Oxnard GR, Janjigian YY, Arcila ME, et al. Maintained sensitivity to EGFR tyrosine kinase inhibitors in EGFR-mutant lung cancer recurring after adjuvant erlotinib or gefitinib. Clin Cancer Res. 2012;17(19):6322–8.CrossRef
5.
Zurück zum Zitat Chen X, Song X, Yue W, et al. Fibulin-5 inhibits Wnt/beta-catenin signaling in lung cancer. Oncotarget. 2015. (Epub ahead of print) Chen X, Song X, Yue W, et al. Fibulin-5 inhibits Wnt/beta-catenin signaling in lung cancer. Oncotarget. 2015. (Epub ahead of print)
6.
Zurück zum Zitat Chen X, Meng J, Yue W, et al. Fibulin-3 suppresses Wnt/beta-catenin signaling and lung cancer invasion. Carcinogenesis. 2012;35(8):1707–16.CrossRef Chen X, Meng J, Yue W, et al. Fibulin-3 suppresses Wnt/beta-catenin signaling and lung cancer invasion. Carcinogenesis. 2012;35(8):1707–16.CrossRef
7.
Zurück zum Zitat Chen Z, Li J, Li QS, et al. Suppression of PPN/MG61 attenuates Wnt/beta-catenin signaling pathway and induces apoptosis in human lung cancer. Oncogene. 2008;27(24):3483–8.CrossRefPubMed Chen Z, Li J, Li QS, et al. Suppression of PPN/MG61 attenuates Wnt/beta-catenin signaling pathway and induces apoptosis in human lung cancer. Oncogene. 2008;27(24):3483–8.CrossRefPubMed
8.
Zurück zum Zitat Clevers H, Nusse R. Wnt/beta-catenin signaling and disease. Cell. 2011;149(6):1192–205.CrossRef Clevers H, Nusse R. Wnt/beta-catenin signaling and disease. Cell. 2011;149(6):1192–205.CrossRef
9.
Zurück zum Zitat Macdonald BT, Semenov MV, He X. SnapShot: Wnt/beta-catenin signaling. Cell. 2007;131(6):1204.CrossRefPubMed Macdonald BT, Semenov MV, He X. SnapShot: Wnt/beta-catenin signaling. Cell. 2007;131(6):1204.CrossRefPubMed
10.
Zurück zum Zitat Clevers H. Wnt/beta-catenin signaling in development and disease. Cell. 2006;127(3):469–80.CrossRefPubMed Clevers H. Wnt/beta-catenin signaling in development and disease. Cell. 2006;127(3):469–80.CrossRefPubMed
11.
Zurück zum Zitat He W, He S, Wang Z, et al. Astrocyte elevated gene-1(AEG-1) induces epithelial-mesenchymal transition in lung cancer through activating Wnt/beta-catenin signaling. BMC Cancer. 2011;15:107.CrossRef He W, He S, Wang Z, et al. Astrocyte elevated gene-1(AEG-1) induces epithelial-mesenchymal transition in lung cancer through activating Wnt/beta-catenin signaling. BMC Cancer. 2011;15:107.CrossRef
12.
Zurück zum Zitat Yang Y, Liu L, Cai J, et al. DEPDC1B enhances migration and invasion of non-small cell lung cancer cells via activating Wnt/beta-catenin signaling. Biochem Biophys Res Commun. 2010;450(1):899–905.CrossRef Yang Y, Liu L, Cai J, et al. DEPDC1B enhances migration and invasion of non-small cell lung cancer cells via activating Wnt/beta-catenin signaling. Biochem Biophys Res Commun. 2010;450(1):899–905.CrossRef
13.
Zurück zum Zitat Teng Y, Wang X, Wang Y, Ma D. Wnt/beta-catenin signaling regulates cancer stem cells in lung cancer A549 cells. Biochem Biophys Res Commun. 2011;392(3):373–9.CrossRef Teng Y, Wang X, Wang Y, Ma D. Wnt/beta-catenin signaling regulates cancer stem cells in lung cancer A549 cells. Biochem Biophys Res Commun. 2011;392(3):373–9.CrossRef
14.
Zurück zum Zitat Nakatani Y, Masudo K, Miyagi Y, et al. Aberrant nuclear localization and gene mutation of beta-catenin in low-grade adenocarcinoma of fetal lung type: up-regulation of the Wnt signaling pathway may be a common denominator for the development of tumors that form morules. Mod Pathol. 2002;15(6):617–24.CrossRefPubMed Nakatani Y, Masudo K, Miyagi Y, et al. Aberrant nuclear localization and gene mutation of beta-catenin in low-grade adenocarcinoma of fetal lung type: up-regulation of the Wnt signaling pathway may be a common denominator for the development of tumors that form morules. Mod Pathol. 2002;15(6):617–24.CrossRefPubMed
15.
Zurück zum Zitat Hneino M, Francois A, Buard V, et al. The TGF-beta/Smad repressor TG-interacting factor 1 (TGIF1) plays a role in radiation-induced intestinal injury independently of a Smad signaling pathway. PLoS One. 2011;7(5):e35672.CrossRef Hneino M, Francois A, Buard V, et al. The TGF-beta/Smad repressor TG-interacting factor 1 (TGIF1) plays a role in radiation-induced intestinal injury independently of a Smad signaling pathway. PLoS One. 2011;7(5):e35672.CrossRef
16.
Zurück zum Zitat Powers SE, Taniguchi K, Yen W, et al. Tgif1 and Tgif2 regulate Nodal signaling and are required for gastrulation. Development. 2011;137(2):249–59.CrossRef Powers SE, Taniguchi K, Yen W, et al. Tgif1 and Tgif2 regulate Nodal signaling and are required for gastrulation. Development. 2011;137(2):249–59.CrossRef
17.
Zurück zum Zitat Richieri-Costa A, Ribeiro LA. Variable phenotypic manifestations of a K44N mutation in the TGIF gene. Brain Dev. 2008;30(3):203–5.CrossRefPubMed Richieri-Costa A, Ribeiro LA. Variable phenotypic manifestations of a K44N mutation in the TGIF gene. Brain Dev. 2008;30(3):203–5.CrossRefPubMed
18.
Zurück zum Zitat Cohen Jr MM. Holoprosencephaly: clinical, anatomic, and molecular dimensions. Birth Defects Res A Clin Mol Teratol. 2006;76(9):658–73.CrossRefPubMed Cohen Jr MM. Holoprosencephaly: clinical, anatomic, and molecular dimensions. Birth Defects Res A Clin Mol Teratol. 2006;76(9):658–73.CrossRefPubMed
19.
Zurück zum Zitat Horie T, Ono K, Kinoshita M, et al. TG-interacting factor is required for the differentiation of preadipocytes. J Lipid Res. 2008;49(6):1224–34.CrossRefPubMed Horie T, Ono K, Kinoshita M, et al. TG-interacting factor is required for the differentiation of preadipocytes. J Lipid Res. 2008;49(6):1224–34.CrossRefPubMed
20.
Zurück zum Zitat Yan L, Womack B, Wotton D, et al. Tgif1 regulates quiescence and self-renewal of hematopoietic stem cells. Mol Cell Biol. 2011;33(24):4824–33.CrossRef Yan L, Womack B, Wotton D, et al. Tgif1 regulates quiescence and self-renewal of hematopoietic stem cells. Mol Cell Biol. 2011;33(24):4824–33.CrossRef
21.
Zurück zum Zitat Hamid R, Brandt SJ. Transforming growth-interacting factor (TGIF) regulates proliferation and differentiation of human myeloid leukemia cells. Mol Oncol. 2009;3(5-6):451–63.CrossRefPubMed Hamid R, Brandt SJ. Transforming growth-interacting factor (TGIF) regulates proliferation and differentiation of human myeloid leukemia cells. Mol Oncol. 2009;3(5-6):451–63.CrossRefPubMed
22.
Zurück zum Zitat Hu ZL, Wen JF, Shen M, Liu Y. Expressions of TGIF, MMP9 and VEGF proteins and their clinicopathological relationship in gastric cancer. Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2006;31(1):70–4.PubMed Hu ZL, Wen JF, Shen M, Liu Y. Expressions of TGIF, MMP9 and VEGF proteins and their clinicopathological relationship in gastric cancer. Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2006;31(1):70–4.PubMed
23.
Zurück zum Zitat Imoto I, Pimkhaokham A, Watanabe T, Saito-Ohara F, Soeda E, Inazawa J. Amplification and overexpression of TGIF2, a novel homeobox gene of the TALE superclass, in ovarian cancer cell lines. Biochem Biophys Res Commun. 2000;276(1):264–70.CrossRefPubMed Imoto I, Pimkhaokham A, Watanabe T, Saito-Ohara F, Soeda E, Inazawa J. Amplification and overexpression of TGIF2, a novel homeobox gene of the TALE superclass, in ovarian cancer cell lines. Biochem Biophys Res Commun. 2000;276(1):264–70.CrossRefPubMed
24.
Zurück zum Zitat Yeh BW, Wu WJ, Li WM, et al. Overexpression of TG-interacting factor is associated with worse prognosis in upper urinary tract urothelial carcinoma. Am J Pathol. 2011;181(3):1044–55.CrossRef Yeh BW, Wu WJ, Li WM, et al. Overexpression of TG-interacting factor is associated with worse prognosis in upper urinary tract urothelial carcinoma. Am J Pathol. 2011;181(3):1044–55.CrossRef
25.
Zurück zum Zitat Zhang MZ, Ferrigno O, Wang Z, et al. TGIF governs a feed-forward network that empowers Wnt signaling to drive mammary tumorigenesis. Cancer Cell. 2012;27(4):547–60.CrossRef Zhang MZ, Ferrigno O, Wang Z, et al. TGIF governs a feed-forward network that empowers Wnt signaling to drive mammary tumorigenesis. Cancer Cell. 2012;27(4):547–60.CrossRef
26.
Zurück zum Zitat Gao Y, Song C, Hui L, et al. Overexpression of RNF146 in non-small cell lung cancer enhances proliferation and invasion of tumors through the Wnt/beta-catenin signaling pathway. PLoS One. 2012;9(1):e85377.CrossRef Gao Y, Song C, Hui L, et al. Overexpression of RNF146 in non-small cell lung cancer enhances proliferation and invasion of tumors through the Wnt/beta-catenin signaling pathway. PLoS One. 2012;9(1):e85377.CrossRef
27.
Zurück zum Zitat Li X, Cai L, Liang M, Wang Y, Yang J, Zhao Y. ING4 induces cell growth inhibition in human lung adenocarcinoma A549 cells by means of Wnt-1/beta-catenin signaling pathway. Anat Rec (Hoboken). 2008;291(5):593–600.CrossRef Li X, Cai L, Liang M, Wang Y, Yang J, Zhao Y. ING4 induces cell growth inhibition in human lung adenocarcinoma A549 cells by means of Wnt-1/beta-catenin signaling pathway. Anat Rec (Hoboken). 2008;291(5):593–600.CrossRef
28.
Zurück zum Zitat Faresse N, Colland F, Ferrand N, Prunier C, Bourgeade MF, Atfi A. Identification of PCTA, a TGIF antagonist that promotes PML function in TGF-beta signalling. Embo J. 2008;27(13):1804–15.CrossRefPubMedPubMedCentral Faresse N, Colland F, Ferrand N, Prunier C, Bourgeade MF, Atfi A. Identification of PCTA, a TGIF antagonist that promotes PML function in TGF-beta signalling. Embo J. 2008;27(13):1804–15.CrossRefPubMedPubMedCentral
29.
Zurück zum Zitat Kim WS, Park C, Hong SK, Park BK, Kim HS, Park K. Microsatellite instability (MSI) in non-small cell lung cancer(NSCLC) is highly associated with transforming growth factor-beta type II receptor(TGF-beta RII) frameshift mutation. Anticancer Res. 2000;20(3A):1499–502.PubMed Kim WS, Park C, Hong SK, Park BK, Kim HS, Park K. Microsatellite instability (MSI) in non-small cell lung cancer(NSCLC) is highly associated with transforming growth factor-beta type II receptor(TGF-beta RII) frameshift mutation. Anticancer Res. 2000;20(3A):1499–502.PubMed
30.
Zurück zum Zitat Cheng T, Hu C, Yang H, Cao L, An J. Transforming growth factor-beta-induced miR143 expression in regulation of non-small cell lung cancer cell viability and invasion capacity in vitro and in vivo. Int J Oncol. 2011;45(5):1977–88. Cheng T, Hu C, Yang H, Cao L, An J. Transforming growth factor-beta-induced miR143 expression in regulation of non-small cell lung cancer cell viability and invasion capacity in vitro and in vivo. Int J Oncol. 2011;45(5):1977–88.
Metadaten
Titel
TGIF1 promoted the growth and migration of cancer cells in nonsmall cell lung cancer
verfasst von
Guo Xiang
Yang Yi
He Weiwei
Wu Weiming
Publikationsdatum
01.12.2015
Verlag
Springer Netherlands
Erschienen in
Tumor Biology / Ausgabe 12/2015
Print ISSN: 1010-4283
Elektronische ISSN: 1423-0380
DOI
https://doi.org/10.1007/s13277-015-3676-8

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