Adiponectin Represses Colon Cancer Cell Proliferation via AdipoR1- and -R2-Mediated AMPK Activation

Kim, A. Young; Lee, Yun Sok; Kim, Kang Ho; Lee, Jae Ho; Lee, Hee Kyu; Jang, Su Hwa; Kim, Seong‐Eun; Lee, Gha Young; Lee, Joowon; Jung, Sung-Ae; Chung, Hee Yong; Jeong, Sunjoo; Kim, Jae Bum

doi:10.1210/jcem.95.5.9995

Cited by 32 publications

(37 citation statements)

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“…In a mouse model, Fujisawa T et al (2008) showed that adiponectin depresses colorectal carcinogenesis and leads the way for further investigations. There is also evidence that adiponectin suppresses colon cancer cells by its receptor mediated AMPK activity (Sugiyama et al, 2009;Kim et al, 2010). In our study plasma adiponectin levels are lower in colon cancer patients than the control group, and this association is statistically significant.…”

Section: Discussionsupporting

confidence: 66%

Associations between Adiponectin and Two Different Cancers: Breast and Colon

Gülçelik¹,

Colakoglu²,

Dincer³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Objectives: Breast and colon cancer are neoplasms well known to be related to obesity. Adiponectin, a protein that increases in obesity, seems to be involved in the relationship but clinical data are limited. Methods: In this study, we therefore evaluated the serum adiponectin levels in 87 breast and 27 colon cancer patients and assessed the relation with BMI, menopausal status, receptor status and stage of disease. Results: Serum adiponectin levels were lower in cancer cases (8583 ± 2095 ng/ml for breast cancer, 9513 ± 2276 for colon cancer) than in controls (13905 ± 3263). Conclusion: A low serum adiponectin level may be associated with both breast and colon cancer, and that this association is not statistically significant for either receptor or menopausal status in breast cancer groups.

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Section: Discussionsupporting

confidence: 66%

Associations between Adiponectin and Two Different Cancers: Breast and Colon

Gülçelik¹,

Colakoglu²,

Dincer³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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“…However, Mather KJ et al (2012) had reported that there was no relationship between ADIPOR1 rs1342387 and adiponectin concentrations. Kim AY et al (Kim et al, 2010) reported that knockdown of ADIPOR1 could relieve the suppressive effect of adiponectin on the growth of colon cancer cells via AMP-activated protein kinase (AMPK) phosphorylation. The association of rs1342387 polymorphism with colorectal cancer risk maybe mainly due to affection of adiponectin function on cellular proliferation and apoptosis, and the direct relationship needs further study.…”

Section: Discussionmentioning

confidence: 99%

“…Adiponectin is involved in anti-inflammatory, insulin-sensitizing, and anti-proliferation activities which are associated with the development of cancer (Barb et al, 2007;Ziemke and Mantzoros, 2010). Recent studies have confirmed that adiponectin implement the main biological function by signaling through its receptors-ADIPOR 1 and ADIPOR Li-Xiang Yu 1 , Nan-Nan Zhou 2 *, Li-Yuan Liu 3 , Fei Wang 1 , Zhong-Bing Ma 1 , Jie Li 4 , Zhi-Gang Yu 1 2 (Kim et al, 2010), which are expressed in various of malignancies including colorectal cancer, breast cancer, prostate cancer and so on (Kim et al, 2010;Dalamaga et al, 2012). The higher expression of AdipoR1, the stronger growth inhibitory effect of adiponectin was observed in cancer cell lines (Tsukada et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

“…A down-regulation of AdipoR1 by specific siRNA could also significantly suppress the antiproliferative effects of adiponectin (Ishikawa et al, 2007). Although the functional of adiponectin receptors in cancer cells has not been fully explained, the AMP-activated protein kinase (AMPK) may play an important role in the limits of cancer cell lines proliferation by adiponectin and its receptors (Kim et al, 2010). In addition, genetic factors, such as genetic polymorphism, could play an extremely important role in cancer susceptibility.…”

Section: Introductionmentioning

confidence: 99%

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Adiponectin Receptor 1 (ADIPOR1) rs1342387 Polymorphism and Risk of Cancer: a Meta-analysis

Cui

Zhou²,

Liu³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Asian Pac J Cancer Prev, 15 (18), 7515-7520 IntroductionCancer and obesity are two major public health problems of this century. In 2008, an estimated 12.7 million new cancer cases and 7.6 million cancer deaths occurred all over the world (Ferlay et al., 2010), and in the same year, about 1.46 billion adults were overweight worldwide, of whom estimated 500 million adults were obese (Finucane et al., 2011). Epidemiological studies had established that increasing of BMI and excess body weight were risk factors for some cancers, such as colorectal cancer, prostate cancer and renal cancer, which were called obesity-related cancers (Renehan et al., 2008;Vucenik and Stains, 2012). Recent studies had revealed that adiponectin, the most abundant adiposetissue protein, was a key player in the development and progression of obesity-related cancers (Barb et al., 2007;Paz-Filho et al., 2011;Liu et al., 2013). Adiponectin is involved in anti-inflammatory, insulin-sensitizing, and anti-proliferation activities which are associated with the development of cancer (Barb et al., 2007;Ziemke and Mantzoros, 2010). Recent studies have confirmed that adiponectin implement the main biological function by signaling through its receptors-ADIPOR 1 and ADIPOR

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“…Several studies have shown the negative effect of adiponectin on the proliferation of several cancer cell lines (144,146). Epidemiological studies, using serum adiponectin level as a measure of tissue exposure, suggested that adiponectin was a protective factor against breast cancer (147)(148)(149)(150)(151).…”

Section: Adiponectin and The Adiponectin Receptorsmentioning

confidence: 99%

Hormonal regulation of immune modulators in human breast tissue

Morad¹

2015

Linköping University Medical Dissertations

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Breast cancer is the most common form of cancer and the second leading cause of malignancy-associated death in women worldwide. Estrogens are the main sex hormones in women. They are essential for the development and function of normal breast mammary glands; however, prolonged exposure to estrogens increases the risk of breast cancer development and progression. Approximately two-thirds of all breast cancer patients are positive for estrogen receptor (ER), but only 50% of those cases can benefit from antiestrogen therapy. In this thesis we investigated the effects of estrogen, diet modification, and anti-estrogen drugs on several immune modulators in normal human breast tissue. We used the microdialysis technique to sample the immune modulators in situ in normal human breast tissue, in malignant breast tissue, and in tumor tissue from both the immune competent mice with murine breast cancer and immune deficient mice bearing human breast tumors. Furthermore, we also used ex vivo culture of normal breast tissue and in vitro cell culture of breast cancer cell lines. A combined cell culture (co-culture) of breast cancer cell lines, together with the primary mature adipocytes, was also used in this thesis. In Paper I and Paper II, our results suggested that estrogen exerted both proinflammatory and pro-tumorigenic effects in normal human breast tissue. Estradiol increased extracellular interleukin-1β (IL-1β) and leptin levels and decreased IL-1Ra and adiponectin levels in normal human breast tissue. In contrast, tamoxifen decreased IL-1β and leptin levels and increased IL-1Ra and adiponectin levels, shifting the environment towards an antiinflammatory and antitumorigenic state. Diet modification with flaxseed for 30 days also increased IL-1Ra levels, creating an anti-inflammatory environment in normal breast tissue. In the breast cancer tissue, we found that extracellular IL-1β levels and leptin levels were significantly higher, whereas adiponectin levels were significantly lower, compared with normal adjacent breast tissue, which suggested a more proinflammatory state. In the third paper, our in vivo investigation of normal breast tissue revealed significant correlations between vascular endothelial growth factor (VEGF) and leptin, IL-1β and leptin, and between VEGF and IL-1β. No correlations were found in the abdominal subcutaneous (s.c.) fat tissue. Our in vitro inhibition experiments suggested that VEGF was a potent regulator of leptin, but that leptin was not a potent regulator of VEGF. Co-culture per se altered the release of VEGF and leptin and enhanced the effects of estradiol, compared with monocultures of the included cell types. In conclusion, the results presented in this thesis will increase the overall understanding of the role of estrogens in breast cancer, which may be useful in future treatment studies

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Adiponectin Represses Colon Cancer Cell Proliferation via AdipoR1- and -R2-Mediated AMPK Activation

Cited by 32 publications

References 0 publications

Associations between Adiponectin and Two Different Cancers: Breast and Colon

Associations between Adiponectin and Two Different Cancers: Breast and Colon

Adiponectin Receptor 1 (ADIPOR1) rs1342387 Polymorphism and Risk of Cancer: a Meta-analysis

Hormonal regulation of immune modulators in human breast tissue

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