Demonstration of Adiponectin Receptors 1 and 2 mRNA expression in human breast cancer cells

Takahata, Chie; Miyoshi, Yasuo; Irahara, Natsumi; Taguchi, Tetsuya; Tamaki, Yasuhiro; Noguchi, Shinzaburo

doi:10.1016/j.canlet.2006.10.006

Cited by 82 publications

(72 citation statements)

References 28 publications

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“…Acrp30 is found at high concentrations (2-20 mg ml À1 ) in human serum (Arita et al, 1999;Bondanelli et al, 2001;Miyoshi et al, 2003;Mantzoros et al, 2004;Chen et al, 2006;Korner et al, 2007;Takahata et al, 2007). There are several different forms of Acrp30 in plasma that bind with varying affinity to the two different Acrp30 receptors, AdipoR1, and AdipoR2 (Yamauchi et al, 2003a).…”

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confidence: 99%

Effects of adiponectin on breast cancer cell growth and signaling

et al. 2008

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Obesity is a risk factor for postmenopausal breast cancer. Adiponectin/Acrp30 is lower in obese individuals and may be negatively regulating breast cancer growth. Here we determined that five breast cancer cell lines, MDA-MB-231, MDA-MB-361, MCF-7, T47D, and SK-BR-3, expressed one or both of the Acrp30 receptors. In addition, we found that the addition of Acrp30 to MCF-7, T47D, and SK-BR-3 cell lines inhibited growth. Oestrogen receptor (ER) positive MCF-7 and T47D cells were inhibited at lower Acrp30 concentrations than ER-negative SK-BR-3 cells. Growth inhibition may be related to apoptosis since PARP cleavage was increased by Acrp30 in the ER-positive cell lines. To investigate the role of ER in the response of breast cancer cells to Acrp30, we established the MDA-ERa7 cell line by insertion of ER-a into ER-a-negative MDA-MB-231 cells. This line readily formed tumours in athymic mice and was responsive to oestradiol in vivo. In vitro, MDA-ERa7 cells were growth inhibited by globular Acrp30 while the parental cells were not. This inhibition appeared to be due to blockage of JNK2 signalling. These results provide information on how obesity may influence breast cancer cell proliferation and establish a new model to examine interactions between ER and Acrp30.

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confidence: 99%

Effects of adiponectin on breast cancer cell growth and signaling

et al. 2008

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“…The mechanisms for down-regulation have been the subject of substantial interest. It has been reported that the expression of LATS2 in breast cancer (14), astrocytoma (17), and acute lymphoblastic leukemia (18,19) is down-regulated by hypermethylation of the promoter. In addition, LATS2 mRNA is down-regulated at the post-transcriptional level by microRNA-372 and microRNA-373 in testicular germ cell tumors (20), gastric cancer cells (21), and esophageal cancer cells (22), suggesting that the expression of the LATS2 gene is controlled at the post-transcriptional level as well as the transcriptional level.…”

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confidence: 99%

Stability of the LATS2 Tumor Suppressor Gene Is Regulated by Tristetraprolin

Lee

Kim

et al. 2010

Journal of Biological Chemistry

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LATS2 is a tumor suppressor gene implicated in the control of cell growth and the cell cycle. Here, we investigated the posttranscriptional regulation of LATS2 expression by tristetraprolin (TTP). Our results show that the expression level of LATS2 is inversely correlated with TTP expression in human cancer cell lines. Overexpression of TTP reduced the expression level of LATS2. Conversely, treatment with small interfering RNA against TTP increased the expression level of LATS2 through stabilization of LATS2 mRNA and suppressed the proliferation of A549 human lung cancer cells. LATS2 mRNA contains AUrich elements (AREs) within the 3-untranslated region, and TTP destabilized a luciferase mRNA containing LATS2 ARE. In addition, RNA electrophoretic mobility shift assay revealed that TTP directly bound to the ARE of LATS2 mRNA. These results establish LATS2 mRNA as a physiological target of TTP and suggest the possibility that TTP controls cell growth through regulation of LATS2 mRNA stability.LATS2 is a new member of the LATS tumor suppressor family (1-3). The LATS2 gene is located at chromosome 13q11-12 and encodes a 1046-amino acid protein that contains a C-terminal serine/threonine kinase domain (4). According to recent publications, LATS2 appears to coordinate the cell cycle, cell proliferation, and cell death. LATS2 promotes the stabilization of p53 by inactivating MDM2 (5), plays a role in maintenance of mitotic fidelity (6), and regulates spindle organization through recruitment of ␥-tubulin to the centrosome (7). Overexpression of LATS2 results in G 2 /M arrest via inhibition of Cdc2 kinase activity (8), inhibition of G 1 /S transition via down-regulation of cyclin E/Cdk2 kinase activity (9), and induction of apoptosis via down-regulation of apoptotic inhibitors such as Bcl-2 and Bcl-x L (10). Deletion of LATS2 in flies (11, 12) and mice (13) accelerates cell proliferation and tumor development, indicating that the reduced function of the LATS2 gene leads to accelerated cell proliferation.Expression of LATS2 is down-regulated in several human cancer cells (14 -18). The mechanisms for down-regulation have been the subject of substantial interest. It has been reported that the expression of LATS2 in breast cancer (14), astrocytoma (17), and acute lymphoblastic leukemia (18, 19) is down-regulated by hypermethylation of the promoter. In addition, LATS2 mRNA is down-regulated at the post-transcriptional level by microRNA-372 and microRNA-373 in testicular germ cell tumors (20), gastric cancer cells (21), and esophageal cancer cells (22), suggesting that the expression of the LATS2 gene is controlled at the post-transcriptional level as well as the transcriptional level.Post-transcriptional regulation of gene expression is also mediated by AU-rich elements (AREs) 4 located in the 3Ј-untranslated region (3Ј-UTR) of a variety of short-lived mRNAs such as cytokines and proto-oncogenes (23). The destabilizing function of AREs is believed to be regulated by ARE-binding proteins (24). Numerous ARE-binding proteins ha...

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“…In this study, we examined the effects of adiponectin on proliferation and gene expression of immortalised mammary epithelial cells in comparison with breast cancer cells. Recently, expression of both AdipoR was reported to be present in various benign mammary epithelial and breast cancer cell lines (Takahata et al, 2007). In this study, mRNA levels of AdipoR1 and AdipoR2 were shown to be expressed in a similar range in MCF-7 and MCF-10A cells.…”

Section: Discussionmentioning

confidence: 55%

Adiponectin differentially affects gene expression in human mammary epithelial and breast cancer cells

et al. 2008

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Serum levels of adiponectin are inversely associated with breast cancer risk. In this study, its effect on growth and gene expression of MCF-7 breast cancer cells and MCF-10A human mammary epithelial cells was compared. The antiproliferative effect of adiponectin on MCF-10A cells was more pronounced and was accompanied by elevated transcript levels of caspase 1, ERb2, ERb5, TR2 and USP2. Our data suggest that upregulation of genes with known growth inhibitory or apoptotic functions in mammary epithelial cells might contribute to the protective action of this adipocytokine.

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Demonstration of Adiponectin Receptors 1 and 2 mRNA expression in human breast cancer cells

Cited by 82 publications

References 28 publications

Effects of adiponectin on breast cancer cell growth and signaling

Effects of adiponectin on breast cancer cell growth and signaling

Stability of the LATS2 Tumor Suppressor Gene Is Regulated by Tristetraprolin

Adiponectin differentially affects gene expression in human mammary epithelial and breast cancer cells

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