Adiponectin activates c-Jun NH2-terminal kinase and inhibits signal transducer and activator of transcription 3

Miyazaki, Toshiaki; Bub, Jeffrey D.; Uzuki, Miwa; Iwamoto, Yoshiki

doi:10.1016/j.bbrc.2005.05.076

Cited by 114 publications

(84 citation statements)

References 45 publications

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“…More recently, c-Jun NH2-terminal kinase (JNK) and signal transducer and activator of transcription 3 (STAT3) were also shown to be downstream effectors of adiponectin (Miyazaki et al, 2005).…”

Section: Mechanisms That May Link Adiponectin With Carcinogenesismentioning

confidence: 99%

“…It was recently demonstrated that adiponectin stimulates JNK activation in prostate cancer (DU145, PC-3 and LNCaP-FGC cells), hepatocellular carcinoma (HepG2) cells and C2C12 myoblasts, but also drastically suppresses STAT3 activation in DU145 and HepG2 cells, in which STAT3 is constitutively activated (Miyazaki et al, 2005). This suggests that adiponectin may affect the pathogenesis of prostate and hepatocellular carcinomas, which express AdipoR1 and R2 receptors, by acting on tumour cells directly through modulation of JNK and STAT3 (Miyazaki et al, 2005). More studies are needed to further elucidate this area.…”

Section: Mechanisms That May Link Adiponectin With Carcinogenesismentioning

confidence: 99%

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Adiponectin and cancer: a systematic review

2006

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Recent studies have demonstrated that obesity is a significant risk factor for the development of several malignancies, but the mechanisms underlying this relationship remain to be fully elucidated. Adiponectin, an adipocyte secreted endogenous insulin sensitizer, appears to play an important role not only in glucose and lipid metabolism but also in the development and progression of several obesity-related malignancies. In this review, we present recent findings on the association of adiponectin with several malignancies as well as recent data on underlying molecular mechanisms that provide novel insights into the association between obesity and cancer risk. We also identify important research questions that remain unanswered.

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Section: Mechanisms That May Link Adiponectin With Carcinogenesismentioning

confidence: 99%

Section: Mechanisms That May Link Adiponectin With Carcinogenesismentioning

confidence: 99%

Adiponectin and cancer: a systematic review

2006

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“…27 Globular adiponectin, a proteolytic product devoid of the collagen domain, has similar effects to full-length adiponectin in some cellular contexts, best shown by studies of tumor cell lines. 35 In cardiac muscle from newborn rabbits, the globular form regulates fatty acid oxidation, whereas the full-length form has no effect. 36 …”

Section: Adiponectin: Structure and Functionmentioning

confidence: 99%

The ‘beneficial’ adipokines in reproduction and fertility

et al. 2007

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The objective of this study was to review the available information on the signaling proteins produced by adipose tissue in the context of their role in regulating reproductive processes, including ovarian and uterine function. It is well known that both obesity and excessive leanness are associated with reproductive dysfunction. Adipokines are cytokines predominately or exclusively expressed by adipose tissue that circulate and affect target tissues. Four known adipokines, adiponectin, visfatin/ PBEF, omentin and vaspin, all increase tissue sensitivity to insulin, and are thus described as 'beneficial'. There is strong support for a role for adiponectin in the function of the ovary and placenta. There is evidence for direct effects of this adipokine on the late stages of folliculogenesis, and additive interactions of adiponectin with insulin and gonadotropins in inducing periovulatory changes in ovarian follicles. In addition, clinical and genomic studies associate hypoadiponectinemia with obesity-related reproductive disorders, including the polycystic ovarian syndrome. The roles for visfatin/PBEF, omentin and vaspin in reproduction remain to be established. The conclusion thus drawn is that the expression of insulin-sensitizing adipokines varies with adipose abundance. These adipokines have demonstrated both the potential effects on ovarian function and the possible effects on the formation of the placenta, acting through multiple mechanisms.

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“…However, at least one report suggested that ADPN only diminished the proliferation rate of MCF7 cells but did not cause apoptosis (Arditi et al 2007). Furthermore, ADPN reportedly reduced the growth of prostate cancer cell (Miyazaki et al 2005;Bub et al 2006). These various studies have showed that f-Ad and g-Ad can activate JNK in prostate cancer cell Du145, PC-3, LNCaP-FGC and inactivated the STAT3 in DU145 and liver cell HepG2.…”

Section: Discussionmentioning

confidence: 94%

“…Furthermore, ADPN has also been shown to inhibit cell proliferation and induce apoptosis of leukemia and endothelial cells (Yokota et al 2010;Brĺkenhielm et al 2004). Studies have demonstrated that prostate cancer cells such as DU145, PC-3 and LNCaP-FGC express ADPN receptors (Miyazaki et al 2005) and ADPN can also inhibit prostate cancer cell growth (Miyazaki et al 2005). In addition, some research groups have reported that breast cancer cells also express AdipoR1 and AdipoR2 and ADPN is able to mediate the proliferation of breast cancer cells directly through its receptors (Kang et al 2005;Dieudonne et al 2006;Arditi et al 2007;Körner et al 2007;Nakayama et al 2008;Pfeiler et al 2010).…”

Section: Introductionmentioning

confidence: 99%

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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Adiponectin activates c-Jun NH2-terminal kinase and inhibits signal transducer and activator of transcription 3

Cited by 114 publications

References 45 publications

Adiponectin and cancer: a systematic review

Adiponectin and cancer: a systematic review

The ‘beneficial’ adipokines in reproduction and fertility

Adiponectin induces growth inhibition and apoptosis in cervical cancer HeLa cells

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