Adiponectin induces growth arrest and apoptosis of MDA-MB-231 breast cancer cell

Kang, Jee Hyun; Lee, Yoon Young; Yu, Byung Yeon; Yang, Beomjoo; Cho, Kyung Hwan; Yoon, Daekeun; Roh, Yong Kyun

doi:10.1007/bf02978210

Cited by 149 publications

(124 citation statements)

References 25 publications

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“…Several groups reported previously that MDA-MB-231 cells were growth inhibited by Acrp30 (Kang et al, 2005;Wang et al, 2007). However, in our hands proliferation of this cell line was not statistically inhibited by the addition of Acrp30.…”

Section: Discussioncontrasting

confidence: 78%

“…This was suggested by the increase in cleaved caspase-8 and cleaved PARP in these cells. Other reports have found that apoptosis is involved in growth inhibition by Acrp30 by the use of TUNEL or annexin V assays (Kang et al, 2005;Dieudonne et al, 2006;Wang et al, 2006). We have extended those earlier observations by identifying increased cleavage of caspase-8 and PARP following treatment with Acrp30.…”

Section: Discussionsupporting

confidence: 75%

“…Overweight or obese individuals usually have elevated levels of the growth factor leptin, which is positively correlated to body mass index while Acrp30 is negatively correlated with body mass index. We and others are now showing that Acrp30 may be an important negative regulator of breast cancer cell growth (Miyoshi et al, 2003;Kang et al, 2005;Dieudonne et al, 2006). In particular, we are trying to assess the interrelationship of these two adipokines on tumour growth and development.…”

Section: Discussionmentioning

confidence: 99%

“…In vitro assays have indicated that the addition of Acrp30 to the human MDA-MB-231 breast cancer cell line-induced growth arrest and promoted apoptosis (Kang et al, 2005;Wang et al, 2006). Addition of Acrp30 also blocked phosphorylation of Akt and reduced the expression of cyclin D1 (Wang et al, 2006).…”

mentioning

confidence: 99%

“…It has also been reported that under some conditions the normal response of T47D human breast cancer cells to the growth factors in serum can be blocked by Acrp30. In addition, Acrp30 was reported to have some effect on growth inhibition of two other cell lines, Hs578T and SK-BR-3, but no effect on the growth of MCF-7 and HCC-38 cells (Kang et al, 2005). However, other publications found that growth of MCF-7 cells was negatively regulated by Acrp30 (Dieudonne et al, 2006;Arditi et al, 2007) and one of these studies indicated that apoptosis was induced (Dieudonne et al, 2006).…”

mentioning

confidence: 99%

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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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Section: Discussioncontrasting

confidence: 78%

Section: Discussionsupporting

confidence: 75%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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confidence: 99%

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Effects of adiponectin on breast cancer cell growth and signaling

et al. 2008

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Effect of adiponectin on apoptosis: Proapoptosis or antiapoptosis?

Sun¹,

Chen²

2010

BioFactors

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Adiponectin is a protein hormone mainly secreted by adipose tissue that regulates energy homeostasis and glucose and lipid metabolism. Compared with other adipose-derived hormones, adiponectin is very abundant in plasma and is proposed to be a convenient biomarker for many diseases. A large number of in vitro and in vivo studies support the beneficial effects of adiponectin on metabolic syndrome, diabetes, and atherosclerosis. However, the protective actions were challenged occasionally by the controversies in its role in inflammation and in the specific functions of its different conformations. Recently, quite a few reports suggested that the antiapoptotic activity of adiponectin might contribute to its therapeutic potential during ischemia/reperfusion injury in vivo, whereas some studies demonstrated that adiponectin induced apoptosis both in vitro and in vivo. Herein, this review attempts to summarize the present consensus and divergence and to provide possible alternative and/or complementary explanations for this apparent paradox.

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Genetic variants in one‐carbon metabolism‐related genes contribute to NSCLC prognosis in a Chinese population

Jin

Huang

et al. 2010

Cancer

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BACKGROUND: One-carbon metabolism plays a critical role in DNA methylation and DNA synthesis. Variants of genes involved in one-carbon metabolism may result in aberrant methylation and/or DNA synthesis inhibition, and ultimately modulate the initiation and progression of tumors. In this study, the authors hypothesized that polymorphisms in one-carbon metabolism-related genes may contribute to the prognosis of nonsmall cell lung cancer (NSCLC). METHODS: The authors screened 57 potentially functional single nucleotide polymorphisms (SNPs) from 11 candidate genes involved in one-carbon metabolism and genotyped them in a cohort of 568 NSCLC patients by using Illumina Golden Gate platform. The Kaplan-Meier method with log-rank test and Cox proportional hazards model were used for survival analyses. RESULTS: Variant alleles were significantly associated with favorable survivals of NSCLC for MTR rs3768160 A>G (allelic hazards ratio [HR], 0.78; 95% confidence interval [CI], 0.62-0.98), MTRR rs2966952 G>A (allelic HR, 0.84; 95% CI, 0.71-0.99) and DHFR rs1650697 G>A (allelic HR, 0.83; 95% CI, 0.70-0.99) and with unfavorable prognosis for MTHFD1 rs1950902 G>A with borderline significance (allelic HR, 1.18; 95% CI, 0.99-1.40). In addition, the combined genotypes of these four SNPs showed a locus-dosage effect on NSCLC survival (P trend ¼ 6.9 Â 10 À5 ). In the final multivariate Cox regression model, combined genotypes based on 3 categories may be an independent prognostic factor for NSCLC with adjusted trend HR of 0.78 (95% CI, 0.66-0.92). CONCLUSION: Genetic variants in one-carbon metabolism pathway may be candidate biomarkers for NSCLC prognosis. Cancer 2010;116:5700-9.

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Adiponectin induces growth arrest and apoptosis of MDA-MB-231 breast cancer cell

Cited by 149 publications

References 25 publications

Effects of adiponectin on breast cancer cell growth and signaling

Effects of adiponectin on breast cancer cell growth and signaling

Effect of adiponectin on apoptosis: Proapoptosis or antiapoptosis?

Genetic variants in one‐carbon metabolism‐related genes contribute to NSCLC prognosis in a Chinese population

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