Evolving role of adiponectin in cancer-controversies and update

Katira, Arnav; Tan, Peng

doi:10.20892/j.issn.2095-3941.2015.0092

Cited by 78 publications

(67 citation statements)

References 117 publications

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“…Similar to our results, APN ameliorates H 2 O 2 -induced autophagy in cardiomyocytes, moreover, loss of APN enhances autophagy in response to Ang-II infusion in vivo 30 . Therefore, APN modulation of mitophagy seems to be context and cell-type dependent, which is similar to its effects on other signaling pathways 53 .…”

Section: Discussionmentioning

confidence: 77%

Adiponectin modulates oxidative stress-induced mitophagy and protects C2C12 myoblasts against apoptosis

Ren

Yan

et al. 2017

Sci Rep

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Adiponectin (APN), also known as apM1, Acrp30, GBP28 and adipoQ, is a circulating hormone that is predominantly produced by adipose tissue. Many pharmacological studies have demonstrated that this protein possesses potent anti-diabetic, anti-atherogenic and anti-inflammatory properties. Although several studies have demonstrated the antioxidative activity of this protein, the regulatory mechanisms have not yet been defined in skeletal muscles. The aim of the present study was to examine the cytoprotective effects of APN against damage induced by oxidative stress in mouse-derived C2C12 myoblasts. APN attenuated H2O2-induced growth inhibition and exhibited scavenging activity against intracellular reactive oxygen species that were induced by H2O2. Furthermore, treating C2C12 cells with APN significantly induced heme oxygenase-1 (HO-1) and nuclear factor-erythroid 2 related factor 2 (Nrf2). APN also suppressed H2O2-induced mitophagy and partially inhibited the colocalization of mitochondria with autophagosomes/lysosomes, correlating with the expression of Pink1 and Parkin and mtDNA. Moreover, APN protected C2C12 myoblasts against oxidative stress-induced apoptosis. Furthermore, APN significantly reduced the mRNA and protein expression levels of Bax. These data suggest that APN has a moderate regulatory role in oxidative stress-induced mitophagy and suppresses apoptosis. These findings demonstrate the antioxidant potential of APN in oxidative stress-associated skeletal muscle diseases.

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Section: Discussionmentioning

confidence: 77%

Adiponectin modulates oxidative stress-induced mitophagy and protects C2C12 myoblasts against apoptosis

Ren

Yan

et al. 2017

Sci Rep

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“…Adiponectin concentration is inversely correlated with body mass index. Indeed, unlike most of the other adipokines, plasma adiponectin levels are found to be lower in obese individuals than in lean individuals (8,(10)(11)(12).…”

mentioning

confidence: 94%

“…A significant increased relationship has been found between adiponectin levels and breast cancer risk (8). Adiponectin, a hormone mainly produced in adipose tissue, is abundant in human plasma and has been described as an insulin-sensitizing adipocytokine (9,10).…”

mentioning

confidence: 99%

Uncoupling effects of estrogen receptor α on LKB1/AMPK interaction upon adiponectin exposure in breast cancer

et al. 2018

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Adipose tissue is a metabolic and endocrine organ that secretes bioactive molecules called adipocytokines. Among these, adiponectin has a crucial role in obesity-associated breast cancer. The key molecule of adiponectin signaling is AMPK, which is mainly activated by liver kinase B1 (LKB1). Here, we demonstrated that estrogen receptor-α (ERα)/LKB1 interaction may negatively interfere with the LKB1 capability to phosphorylate AMPK and inhibit its downstream signaling TSC2/mTOR/p70S6k. In adiponectin-treated MCF-7 cells, AMPK signaling was not working, resulting in its downstream target acetyl-CoA carboxylase (ACC) being still active. In contrast, in MDA-MB-231 cells, AMPK and ACC phosphorylation was enhanced by adiponectin, inhibiting lipogenesis and cell growth. Upon adiponectin, ERα signaling switched the energy balance of breast cancer cells toward a lipogenic phenotype. Therefore, adiponectin played an inhibitory role on ERα-negative cell growth and progression in vitro and in vivo. In contrast, low adiponectin levels, similar to those circulating in obese patients, acted on ERα-positive cells as a growth factor, stimulating proliferation. The latter effect was blunted in vivo by high adiponectin concentration. All this may have translational relevance, addressing how the handling of adiponectin, as a therapeutic tool in breast cancer treatment, needs to be carefully considered in ERα-positive obese patients, where circulating levels of this adipocytokine are relatively low. In other words, in ERα-positive breast cancer obese patients, higher adiponectin doses should be administered with respect to ERα-negative breast cancer, also opportunely combined with antiestrogen therapy. -Mauro, L., Naimo, G. D., Gelsomino, L., Malivindi, R., Bruno, L., Pellegrino, M., Tarallo, R., Memoli, D., Weisz, A., Panno, M. L., Andò, S. Uncoupling effects of estrogen receptor α on LKB1/AMPK interaction upon adiponectin exposure in breast cancer.

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“…Evidence from experimental studies strongly supports the role of adiponectin in many types of cancers, including those of the breast, colorectum, kidney, liver, pancreas, thyroid, myeloma, stomach, esophagus, and prostate . However, observational studies on the relationship of prediagnostic circulating adiponectin levels with the risk of several cancers have reported mixed results …”

Section: Global Burden Of Cancers Attributable To Excess Body Weightmentioning

confidence: 99%

Global patterns in excess body weight and the associated cancer burden

Sung¹,

Siegel

Torre

et al. 2018

CA A Cancer J Clinicians

385

292

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The prevalence of excess body weight and the associated cancer burden have been rising over the past several decades globally. Between 1975 and 2016, the prevalence of excess body weight in adults—defined as a body mass index (BMI) ≥ 25 kg/m2—increased from nearly 21% in men and 24% in women to approximately 40% in both sexes. Notably, the prevalence of obesity (BMI ≥ 30 kg/m2) quadrupled in men, from 3% to 12%, and more than doubled in women, from 7% to 16%. This change, combined with population growth, resulted in a more than 6‐fold increase in the number of obese adults, from 100 to 671 million. The largest absolute increase in obesity occurred among men and boys in high‐income Western countries and among women and girls in Central Asia, the Middle East, and North Africa. The simultaneous rise in excess body weight in almost all countries is thought to be driven largely by changes in the global food system, which promotes energy‐dense, nutrient‐poor foods, alongside reduced opportunities for physical activity. In 2012, excess body weight accounted for approximately 3.9% of all cancers (544,300 cases) with proportion varying from less than 1% in low‐income countries to 7% or 8% in some high‐income Western countries and in Middle Eastern and Northern African countries. The attributable burden by sex was higher for women (368,500 cases) than for men (175,800 cases). Given the pandemic proportion of excess body weight in high‐income countries and the increasing prevalence in low‐ and middle‐income countries, the global cancer burden attributable to this condition is likely to increase in the future. There is emerging consensus on opportunities for obesity control through the multisectoral coordinated implementation of core policy actions to promote an environment conducive to a healthy diet and active living. The rapid increase in both the prevalence of excess body weight and the associated cancer burden highlights the need for a rejuvenated focus on identifying, implementing, and evaluating interventions to prevent and control excess body weight.

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Evolving role of adiponectin in cancer-controversies and update

Cited by 78 publications

References 117 publications

Adiponectin modulates oxidative stress-induced mitophagy and protects C2C12 myoblasts against apoptosis

Adiponectin modulates oxidative stress-induced mitophagy and protects C2C12 myoblasts against apoptosis

Uncoupling effects of estrogen receptor α on LKB1/AMPK interaction upon adiponectin exposure in breast cancer

Global patterns in excess body weight and the associated cancer burden

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