The regulation of adiponectin receptors in human prostate cancer cell lines

Mistry, Tına; Digby, Janet E.; Chen, Jing; Desai, Ken; Randeva, Harpal S.

doi:10.1016/j.bbrc.2006.07.139

Cited by 67 publications

(49 citation statements)

References 26 publications

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“…RT-PCR confirmed that HeLa cells express ADPN receptors, and further demonstrated that the expression level of AdipoR2 mRNA was up-regulated in HeLa cells treated with ADPN. This is similar to reports that g-Ad stimulated the expression of AdipoR2 mRNA in prostate cancer cells (Mistry et al 2006). The MTT assay showed that ADPN inhibits proliferation of HeLa cells in a concentration-and time-dependent manner.…”

Section: Discussionsupporting

confidence: 91%

Adiponectin induces growth inhibition and apoptosis in cervical cancer HeLa cells

Xie

Wang

et al. 2011

Biologia

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Obesity is a known risk factor for postmenopausal cervical cancer. In human, plasma adiponectin (ADPN) levels are inversely associated with obesity. ADPN may influence the pathogenesis of cervical cancer. In this paper, the effects of ADPN on the proliferation of the cervical cancer HeLa cells and its underlying mechanism were studied. We discovered that two ADPN receptors were expressed in HeLa cells and ADPN inhibited the proliferation of HeLa cells. Western-blotting showed that ADPN activated AMP kinase in HeLa cells. Reverse transcriptase-polymerase chain reaction revealed ADPN down-regulated the expression of cell cycle regulators cyclin D1 and c-myc, and induced the expression of p21 WAF1/CIP1 and p53. These results indicate that ADPN inhibits proliferation and induces apoptosis of HeLa cells by altering the expression of cell cycle regulators.

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Section: Discussionsupporting

confidence: 91%

Adiponectin induces growth inhibition and apoptosis in cervical cancer HeLa cells

Xie

Wang

et al. 2011

Biologia

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“…Adiponectin is indeed able to downregulate its own receptors, AdipoR1 and AdipoR2. These downregulations have already been observed in different tissues and cell lines (adipose tissue, prostate cancer cell lines, and MDA-MB 231 mammary cancer cells) (Bauche et al 2006, Dos Santos et al 2008) and more particularly in human placenta (Caminos et al 2005, Mistry et al 2006. In trophoblastic cell line BeWo, we recently described that adiponectin inhibited AdipoR mRNA expression at the low concentration of 25 ng/ml (Benaitreau et al 2010).…”

Section: Discussionmentioning

confidence: 76%

Effects of adiponectin on human trophoblast invasion

Benaîtreau¹,

Santos²,

Leneveu³

et al. 2010

Journal of Endocrinology

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Adiponectin is an adipokine with insulin-sensitizing, antiinflammatory, anti-atherogenic, and anti-proliferative effects. The expression of specific adiponectin receptors in the placenta and in the endometrium suggests a role for this cytokine in placental development, but this role has not yet been elucidated. The invasion of trophoblast cells during the first trimester of pregnancy being crucial to placentation process, we have studied adiponectin effects on human trophoblast invasive capacities. We found that adiponectin stimulated human trophoblast cell migration in HTR-8/SVneo cells in a dose-independent manner. In addition, adiponectin also significantly enhanced invasion of HTR-8/SVneo cells and of human extravillous trophoblast from first trimester placenta. These pro-invasive effects of adiponectin in human trophoblasts seem to be mediated in part via increased matrix metalloproteinases (MMP2 and MMP9) activities and via repression of TIMP2 mRNA expression. Our results suggest that adiponectin could be a positive regulator of the early invasion process by modulating the MMP/TIMP balance. Moreover, these results provide an insight into the role of adiponectin in pathological conditions characterized by insufficient or excessive trophoblast invasion.

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“…One prospective study showed that low adiponectin levels correlated with increased risk for colorectal cancer (Wei et al 2005), while another study in a different population did not confirm this finding (Lukanova et al 2006). The two putative adiponectin receptors (AdipoR1 and AdipoR2) are highly expressed not only in metabolically active organs, i.e., skeletal muscle, liver, adipose tissue, pancreas (Yamauchi et al 2003), and more recently in the brain (Ahima 2006), but also in breast (Dieudonne et al 2006), prostate (Miyazaki et al 2005, Bub et al 2006, Mistry et al 2006, and hepatocellular carcinomas (Miyazaki et al 2005). Thus, in addition to its insulin-sensitizing role, adiponectin may also regulate cell proliferation and specific signaling pathways in cancer cells.…”

Section: Introductionmentioning

confidence: 96%

Adiponectin signals in prostate cancer cells through Akt to activate the mammalian target of rapamycin pathway

Barb¹,

Neuwirth²,

Mantzoros³

et al. 2007

Endocrine Related Cancer

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Adiponectin has received much attention due to its beneficial effects on insulin sensitivity, and epidemiologic studies have further shown an inverse association between adiponectin levels and risk for multiple tumors, which is independent of the IGF system or other risk factors. Previous studies have shown that adiponectin can activate AMP-activated protein kinase (AMPK) in myocytes, hepatocytes, and adipocytes, suggesting that adiponectin may suppress tumor development through AMPK activation and subsequent inhibition of mammalian target of rapamycin (mTOR). However, the mechanisms through which adiponectin affects cancer cells are not understood, and it remains to be determined whether adiponectin is linked to the same downstream targets in all cells types, and in particular in cancer cells. In the present study, we demonstrate that while adiponectin stimulates AMPK in phosphatase and tensin homolog deleted on chromosome ten (PTEN) deficient LNCaP prostate cancer cells, it also increases mTOR activity as assessed by phosphorylation of two downstream targets, p70 S6 kinase and ribosomal protein S6. This adiponectin stimulation of mTOR was mediated through phosphatidylinositol 3-kinase (PI3 kinase) and Akt activation. These results show that adiponectin can activate both AMPK and PI3 kinase/Akt pathways, and that cell type-specific factors such as PTEN status may determine which of these pathways will have the dominant effect on mTOR. Therefore, while it is possible that high endogenous adiponectin levels could be protective against cancer by direct mechanisms or indirect systemic mechanisms, our results indicate that adiponectin may also directly stimulate signaling pathways that enhance the growth of some tumors.

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The regulation of adiponectin receptors in human prostate cancer cell lines

Cited by 67 publications

References 26 publications

Adiponectin induces growth inhibition and apoptosis in cervical cancer HeLa cells

Adiponectin induces growth inhibition and apoptosis in cervical cancer HeLa cells

Effects of adiponectin on human trophoblast invasion

Adiponectin signals in prostate cancer cells through Akt to activate the mammalian target of rapamycin pathway

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