Trefoil Factor-1 (TFF1) Enhances Oncogenicity of Mammary Carcinoma Cells

Amiry, N.; Kong, Xiangjun; Muniraj, Nethaji; Kannan, Nagarajan; Grandison, Prudence M.; Lin, Juan; Yang, Yulu; Vouyovitch, Cécile M.; Borgés, Sahra; Perry, Jo K.; Mertani, Hichem C.; Zhu, Tao; Li, Dongxu; Lobie, Peter E.

doi:10.1210/en.2009-0066

Cited by 64 publications

(49 citation statements)

References 60 publications

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“…Both GREB1 and TFF1 are strongly correlated with ER protein expression and are required for E2-induced proliferation and invasion of ERϩ breast cancer cells. 21,32,33 TRIM29 is able to independently induce these ER-regulated genes, but the level of induction is reduced in the presence of E2, accounting for the observed tumor suppressor effects.…”

Section: Discussionmentioning

confidence: 99%

TRIM29 Functions as a Tumor Suppressor in Nontumorigenic Breast Cells and Invasive ER+ Breast Cancer

Liu

Welm

Boucher

et al. 2012

The American Journal of Pathology

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Tripartite motif-containing 29 (TRIM29) is a member of the TRIM protein family that has been implicated in hematologic and solid tumor cancers. We found that TRIM29 functions as a tumor suppressor in both the nontumorigenic MCF10A [estrogen receptor (ER)؊/TRIM29؉] breast cell line and the invasive MCF7 (ER؉/TRIM29؊) breast cell line. Silencing TRIM29 in MCF10A cells resulted in preneoplastic changes that included loss of polarity in three-dimensional culture, increased proliferation, anchorage-independent growth, and increased migration and invasion. Conversely, the introduction of TRIM29 into MCF7 cells caused reversion to a less aggressive phenotype by antagonizing the growth effect of 17␤-estradiol. The interaction between TRIM29 and ER signaling in MCF7 cells was supported by a reduction in ERE binding in the presence of TRIM29 and suppression of ER-dependent gene expression of TFF1, FOS, and GREB1. By microarray analyses, we showed that younger women (<55 years of age) with early-stage, ER؉ breast cancer who were given no adjuvant systemic therapy had a significantly lower risk of relapse when their tumor had high TRIM29 expression (P ‫؍‬ 0.02). This effect was not observed in older women (>55 years of age) and thus may be due to menopause and loss of circulating estrogens. Our results suggest that loss of TRIM29 expression in normal breast luminal cells can contribute to malignant transformation and lead to progression of ER؉ breast cancer in premenopausal women. The ataxia telangiectasia group D-complementing (ATDC/TRIM29) gene was identified by its ability to partially restore the radiosensitive phenotype of cells from patients with ataxia telangiectasia, 1,2 a rare autosomal recessive disease in which patients develop immunodeficiency, neurodegenerative disorders, and cancer. 3 TRIM29 encodes for a member of the tripartite motif (TRIM) protein family, which is generally defined by having an ordered series of three zinc-binding domains, a RING (R) domain, two unique B-box (BB) domains, and a coiled-coiled (CC) region. Although some members of the TRIM family may not contain all domains (eg, TRIM29 has no R domain), the order of the regions is always conserved and is the telltale sign of the TRIM motif. TRIM proteins, including TRIM29, self-interact through the CC domain, and this homo-oligomerization is necessary for appropriate localization to distinct cellular compartments that appear as cytoplasmic or nuclear "bodies." 4 TRIM29 is involved in a variety of cancers; however, its function can change, depending on the cell type, level of expression, posttranslational modification, and compartmentalization. 4,5 Although TRIM29 has been implicated as a tumor suppressor in some types of breast and bone cancers, 6 it is also known to have oncogenic effects in gastric and pancreatic cancers. 7,8 Transfection of wildtype TRIM29 into osteosarcoma and breast cancer cell lines (Saos-2 and BT-549) lacking detectable mRNA and protein expression of TRIM29 results in suppression of colony-forming efficiency in soft ag...

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Section: Discussionmentioning

confidence: 99%

TRIM29 Functions as a Tumor Suppressor in Nontumorigenic Breast Cells and Invasive ER+ Breast Cancer

Liu

Welm

Boucher

et al. 2012

The American Journal of Pathology

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“…Amiry et al showed that TFF1 functioned as an oncogene and forced expression of TFF1 increased the oncogenicity of human breast cancer MCF7 and T47D cells [68]. On the contrary, Buache et al reported TFF1 acted as a beneficial factor rather than an oncogene in the breast and knockout of TFF1 augmented the tumorigenicity of breast cancer cells and stimulated breast tumor development [69]. Although TFF1 enhanced the migration and invasion of breast cancer MDA-MB-231, MCF7 and ZR75.1 cells under in vitro conditions, its expression is usually depleted in highly metastatic breast cancer cell lines such as MDA-MB-231 [69].…”

Section: Riz1 Exerts Its Histone Modification Functions Via Binding Tmentioning

confidence: 99%

Tumor Suppressor RIZ1 in Carcinogenesis

Sun¹,

Yang

2014

J Carcinog Mutagen

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“…Extraction of RNA and semiquantitative RT-PCR RNA extraction and semiquantitative reverse transcriptase (RT)-PCR was carried out as described previously (Amiry et al 2009). Amplified RT-PCR products were visualised on a 1.5% agarose gel.…”

Section: Cell Lines and Cell Transfectionmentioning

confidence: 99%

“…Cell growth in the basement membrane extract, Matrigel, was assayed as described previously (Amiry et al 2009). Briefly, RL95-2, T47D and MDA-MB-435S cells were suspended in 4% growth factor reduced Matrigel (BD Biosciences, San Jose, CA, USA) in 5% serum media in 96-well plates at 1000 cells/well.…”

Section: D Matrigel Assaymentioning

confidence: 99%

Autocrine human GH promotes radioresistance in mammary and endometrial carcinoma cells

Bougen¹,

Steiner²,

Pertziger³

et al. 2012

Endocrine-Related Cancer

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Although recent advances in breast cancer treatment regimes have improved patient prognosis, resistance to breast cancer therapies, such as radiotherapy, is still a major clinical challenge. In the current study, we have investigated the role of autocrine human GH (hGH) in resistance to ionising radiation (IR)-based therapy. Cell viability and total cell number assays demonstrated that autocrine hGH promoted cell regrowth in the mammary carcinoma cell lines, MDA-MB-435S and T47D, and the endometrial carcinoma cell line, RL95-2, following treatment with IR. In addition, autocrine hGH enhanced MDA-MB-435S and T47D cell clonogenic survival following radiation exposure. The enhanced clonogenic survival afforded by autocrine hGH was mediated by JAK2 and Src kinases. Investigation into the DNA repair capacity demonstrated that autocrine hGH reduced IR-induced DNA damage in MDA-MB-435S and T47D cells. Functional antagonism of hGH increased RL95-2 sensitivity to IR in cell viability and total cell number assays, reduced clonogenic survival and enhanced the induction of DNA damage. Thus, autocrine hGH reduced sensitivity to treatment with IR in mammary and endometrial carcinoma cell lines in vitro, while functional antagonism of hGH sensitised endometrial carcinoma cells to IR. Functional antagonism of hGH, used in conjunction with radiotherapy, may therefore enhance treatment efficacy and improve the prognosis of patients with breast and endometrial cancer.

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Trefoil Factor-1 (TFF1) Enhances Oncogenicity of Mammary Carcinoma Cells

Cited by 64 publications

References 60 publications

TRIM29 Functions as a Tumor Suppressor in Nontumorigenic Breast Cells and Invasive ER+ Breast Cancer

TRIM29 Functions as a Tumor Suppressor in Nontumorigenic Breast Cells and Invasive ER+ Breast Cancer

Tumor Suppressor RIZ1 in Carcinogenesis

Autocrine human GH promotes radioresistance in mammary and endometrial carcinoma cells

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