Skip to main content
Key Specialties
Cardiology Diabetology Endocrinology Gastroenterology Geriatrics and Gerontology Gynecology and Obstetrics Hematology Infectious Disease Internal Medicine Nephrology Neurology Oncology Pediatrics Respiratory Medicine Rheumatology Surgery
Congress Coverage
2024 ACC Congress 2023 ESMO Congress 2023 EASD Congress 2023 ERS Congress 2023 ESC Congress
Clinical Collections
Advances in Alzheimer’s

At a glance: The STEP trials

A round-up of the STEP phase 3 clinical trials evaluating semaglutide for weight loss in people with overweight or obesity.
ADVANCED SEARCH
Log in
Top
Tumor Biology
Published in: Tumor Biology 12/2015

01-12-2015 | Research Article

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

Authors: Guo Xiang, Yang Yi, He Weiwei, Wu Weiming

Published in: Tumor Biology | Issue 12/2015

Login to get access

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.
Literature
1.
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.
3.
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.
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.
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.
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.
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.
Clevers H, Nusse R. Wnt/beta-catenin signaling and disease. Cell. 2011;149(6):1192–205.CrossRef
9.
10.
11.
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.
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.
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.
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.
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.
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.
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.
Cohen Jr MM. Holoprosencephaly: clinical, anatomic, and molecular dimensions. Birth Defects Res A Clin Mol Teratol. 2006;76(9):658–73.CrossRefPubMed
19.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
Metadata
Title
TGIF1 promoted the growth and migration of cancer cells in nonsmall cell lung cancer
Authors
Guo Xiang
Yang Yi
He Weiwei
Wu Weiming
Publication date
01-12-2015
Publisher
Springer Netherlands
Published in
Tumor Biology / Issue 12/2015
Print ISSN: 1010-4283
Electronic ISSN: 1423-0380
DOI
https://doi.org/10.1007/s13277-015-3676-8

Other articles of this Issue 12/2015

Tumor Biology 12/2015 Go to the issue

Research Article

Frequent methylation of the KLOTHO gene and overexpression of the FGFR4 receptor in invasive ductal carcinoma of the breast

Research Article

RETRACTED ARTICLE: MicroRNA-133a functions as a tumor suppressor by targeting IGF-1R in hepatocellular carcinoma

Review

N-Methyl-N-nitrosourea as a mammary carcinogenic agent

Research Article

Combination of miRNA and RNA functions as potential biomarkers for gastric cancer

Research Article

Cancer cell-derived IL-8 induces monocytic THP1 cells to secrete IL-8 via the mitogen-activated protein kinase pathway

Research Article

High expression of CD39/ENTPD1 in malignant epithelial cells of human rectal adenocarcinoma
Webinar | 19-02-2024 | 17:30 (CET)

Keynote webinar | Spotlight on antibody–drug conjugates in cancer

Watch now

Antibody–drug conjugates (ADCs) are novel agents that have shown promise across multiple tumor types. Explore the current landscape of ADCs in breast and lung cancer with our experts, and gain insights into the mechanism of action, key clinical trials data, existing challenges, and future directions.

Dr. Véronique Diéras
Prof. Fabrice Barlesi
Developed by: Springer Medicine
Image Credits