CTGF is overexpressed in papillary thyroid carcinoma and promotes the growth of papillary thyroid cancer cells

Cui, Lei; Zhang, Qing; Mao, Zhuo‐Ya; Chen, Jixiang; Wang, Xuqing; Qu, Junle; Zhang, Jianxin; Jin, Dayong

doi:10.1007/s13277-011-0173-6

Cited by 28 publications

(32 citation statements)

References 25 publications

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“…In this regard, our results suggest that Egr-1 is capable to mediate the growth effects induced by E2, OHT, and G-1 through GPER in breast and endometrial cancer cells. Interestingly, we ascertained that Egr-1 regulates the transcription of both CTGF and cyclin D1, which are largely known to exert a main role in the proliferation of cancer cells [20,24,26,[31][32][33]. Our findings are in agreement with previous studies showing that the promoter regions of CTGF (Vivacqua and Maggiolini, unpublished data) and cyclin D1 [33] contain multiple cis-regulatory elements, including Egr-1.…”

Section: Discussionsupporting

confidence: 91%

“…GPER activation leads to the release of heparin-bound epidermal growth factor (HB-EGF) which in turn triggers the epidermal growth factor receptor (EGFR)/ERK transduction pathway [30]. Among the subsequent biological responses, the expression of genes involved in cell proliferation and migration such as the connective tissue growth factor (CTGF) and cyclin D1 has been demonstrated [20,24,26,[31][32][33]. In this vein, it is worth noting that elevated CTGF levels were found in numerous types of carcinomas [34][35][36] and associated with aggressive features of breast cancer cells [37,38].…”

Section: Introductionmentioning

confidence: 99%

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GPER mediates the Egr-1 expression induced by 17β-estradiol and 4-hydroxitamoxifen in breast and endometrial cancer cells

Vivacqua

Romeo

Marco

et al. 2011

Breast Cancer Res Treat

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Early growth response-1 (Egr-1) is an immediate early gene involved in relevant biological events including the proliferation of diverse types of cell tumors. In a microarray analysis performed in breast cancer cells, 17β-estradiol (E2) and the estrogen receptor antagonist 4-hydroxitamoxifen (OHT) up-regulated Egr-1 through the G protein-coupled receptor named GPR30/GPER. Hence, in this study, we aimed to provide evidence regarding the ability of E2, OHT and the selective GPER ligand G-1 to regulate Egr-1 expression and function through the GPER/EGFR/ERK transduction pathway in both Ishikawa (endometrial) and SkBr3 (breast) cancer cells. Interestingly, we demonstrate that Egr-1 is involved in the transcription of genes regulating cell proliferation like CTGF and cyclin D1 and required for the proliferative effects induced by E2, OHT, and G-1 in both Ishikawa and SkBr3 cells. In addition, we show that GPER mediates the expression of Egr-1 also in carcinoma-associated fibroblasts (CAFs). Our data suggest that Egr-1 may represent an important mediator of the biological effects induced by E2 and OHT through GPER/EGFR/ERK signaling in breast and endometrial cancer cells. The results obtained in CAFs provide further evidence regarding the potential role exerted by the GPER-dependent Egr-1 up-regulation in tumor development and progression. Therefore, Egr-1 may be included among the bio-markers of estrogen and antiestrogen actions and may be considered as a further therapeutic target in both breast and endometrial tumors.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

GPER mediates the Egr-1 expression induced by 17β-estradiol and 4-hydroxitamoxifen in breast and endometrial cancer cells

Vivacqua

Romeo

Marco

et al. 2011

Breast Cancer Res Treat

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“…Thyroid cancer is classified into four types: papillary, follicular, medullary, and anaplastic thyroid cancer. Papillary thyroid cancer (PTC) is the most common type, accounting for greater than 80% of all thyroid cancers, and is a major type mainly in young women and children [3, 4]. Understanding the molecular mechanism of the proliferation, migration, and invasion of PTC is important for the development of more effective therapeutic strategies.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-613 inhibits cell growth, migration and invasion of papillary thyroid carcinoma by regulating SphK2

et al. 2016

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MicroRNAs (miRNAs) have emerged as important gene regulators and are recognized as key players in carcinogenesis. In this study, we investigated the biological function and mechanism of miR-613 in the regulation of papillary thyroid cancer (PTC) development. We found that miR-613 was downregulated in PTC cell lines and tissues, and overexpression of miR-613 significantly suppressed PTC cell growth, migration and invasion in vitro and inhibited tumor growth in vivo. We identified the gene for sphingosine kinase 2 (SphK2) as a direct target of miR-613. Overexpression of miR-613 significantly repressed SphK2 expression by directly targeting its 3′-untranslated regions (3′-UTR) and restoration of SphK2 reversed the inhibitory effects of miR-613 on PTC cell growth and invasion. Taken together, our results indicated that miR-613 functions as a tumor suppressor in PTC and its suppressive effect is mediated by repressing SphK2 expression.

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“…The split of CTGF gene expression between adherent and MCTS cells corresponds nicely to earlier data from 10 d RPM and spaceflight experiments, which indicated more mRNA in AD than in MCTS cells [2] and could therefore be a microgravity-dependent process involved in spheroid formation. CTGF was found to be over-expressed in papillary thyroid carcinoma correlating with metastasis, size and clinical stage [23]. It was also suggested to play an important role in angiogenesis and tumorigenesis of prostate cancer [24].…”

Section: Discussionmentioning

confidence: 99%

Spheroid formation of human thyroid cancer cells under simulated microgravity: a possible role of CTGF and CAV1

et al. 2014

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BackgroundMulticellular tumor spheroids (MCTS) formed scaffold-free under microgravity are of high interest for research and medicine. Their formation mechanism can be studied in space in real microgravity or on Earth using ground-based facilities (GBF), which simulate microgravity. On Earth, these experiments are more cost-efficient and easily performable. However, each GBF might exert device-specific and altered superimposingly gravity-dependent effects on the cells.ResultsFTC-133 human thyroid cancer cells were cultivated on a 2D clinostat (CN) and a random positioning machine (RPM) and compared with corresponding 1 g control cells. Harvested cell samples were investigated by microscopy, quantitative realtime-PCR and Multi-Analyte Profiling. Spheroid formation and growth occurred during 72 h of cultivation on both devices. Cytokine secretion and gene activation patterns frequently altered in different ways, when the cells were cultured either on the RPM or the CN. A decreased expression of CAV1 and CTGF in MCTS compared to adherent cells was observed after cultivation on both machines.ConclusionThe development of MCTS proceeds similarly on the RPM and the CN resembling the situation observed under real microgravity conditions, while no MCTS formation was observed at 1 g under identical experimental conditions. Simultaneously, changes in the regulation of CTGF and CAV1 appeared in a comparable manner on both machines. A relationship between these molecules and MCTS formation is discussed.

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CTGF is overexpressed in papillary thyroid carcinoma and promotes the growth of papillary thyroid cancer cells

Cited by 28 publications

References 25 publications

GPER mediates the Egr-1 expression induced by 17β-estradiol and 4-hydroxitamoxifen in breast and endometrial cancer cells

GPER mediates the Egr-1 expression induced by 17β-estradiol and 4-hydroxitamoxifen in breast and endometrial cancer cells

MicroRNA-613 inhibits cell growth, migration and invasion of papillary thyroid carcinoma by regulating SphK2

Spheroid formation of human thyroid cancer cells under simulated microgravity: a possible role of CTGF and CAV1

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