Adiponectin as a potential tumor suppressor inhibiting epithelial‐to‐mesenchymal transition but frequently silenced in prostate cancer by promoter methylation

Tan, Wenyong; Wang, Lin; Ma, Quanping; Qi, Mei; Lü, Ning; Zhang, Lili; Han, Bo

doi:10.1002/pros.23002

Cited by 33 publications

(32 citation statements)

References 35 publications

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“…Cells tend to have stronger replicative capacity in the condition of adiponectin deficiency, this capacity is limited and controllable. Although several studies have found correlative evidence between adiponectin deficiency and cancers25, including breast cancer42, hepatocellular carcinoma43 and prostate cancer44. Additional studies are needed to determine whether adiponectin deficiency contributes to the limitless replicative potential of cancer cells.…”

Section: Discussionmentioning

confidence: 99%

Adiponectin deficiency contributes to the development and progression of benign prostatic hyperplasia in obesity

et al. 2017

Sci Rep

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The incidence of benign prostatic hyperplasia (BPH) is increasing among obese individuals, but few studies have fully explained the underlying mechanisms. We aimed to elucidate the relationship between obesity and BPH. Herein, we show that in prostatic epithelial and stromal cells, adiponectin exerts multifunctional effects including anti-proliferation, blocking of G1/S-phase progression and the promotion of apoptosis via inhibiting the MEK-ERK-p90RSK axis. Furthermore, we found that a high-fat diet (HFD) led to adiponectin deficiency and microscopic BPH in a mouse model of obesity. And an adiponectin supplement protected the obese mice from microscopic BPH. The present study provides evidence that adiponectin is a protective regulator in the development and progression of BPH and that adiponectin deficiency causally links BPH with obesity.

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Section: Discussionmentioning

confidence: 99%

Adiponectin deficiency contributes to the development and progression of benign prostatic hyperplasia in obesity

et al. 2017

Sci Rep

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“…+/− [107,151] Funding: This work was supported by grants from the Ministero della Salute (Ricerca Corrente L4084, 2016; L4101, 2017).…”

Section: Breast Cancer Progress Leptin Adiponectin Sam68mentioning

confidence: 99%

Leptin, Adiponectin, and Sam68 in Bone Metastasis from Breast Cancer

Maroni

2020

IJMS

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The most serious aspect of neoplastic disease is the spread of cancer cells to secondary sites. Skeletal metastases can escape detection long after treatment of the primary tumour and follow-up. Bone tissue is a breeding ground for many types of cancer cells, especially those derived from the breast, prostate, and lung. Despite advances in diagnosis and therapeutic strategies, bone metastases still have a profound impact on quality of life and survival and are often responsible for the fatal outcome of the disease. Bone and the bone marrow environment contain a wide variety of cells. No longer considered a passive filler, bone marrow adipocytes have emerged as critical contributors to cancer progression. Released by adipocytes, adipokines are soluble factors with hormone-like functions and are currently believed to affect tumour development. Src-associated in mitosis of 68 kDa (Sam68), originally discovered as a protein physically associated with and phosphorylated by c-Src during mitosis, is now recognised as an important RNA-binding protein linked to tumour onset and progression of disease. Sam68 also regulates splicing events and recent evidence reports that dysregulation of these events is a key step in neoplastic transformation and tumour progression. The present review reports recent findings on adipokines and Sam68 and their role in breast cancer progression and metastasis.

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“…Bub et al showed that adiponectin was a growth inhibitor in PCa cells [34]. Further findings indicated that endogenous adiponectin functioned as a tumor suppressor through inhibiting epithelial-to-mesenchymal transition of PCa cells [35]. On the other side, some researchers presented negative results, suggesting that adiponectin may not play an important role in promoting clinically aggressive PCa [36,37].…”

Section: Discussionmentioning

confidence: 95%

Maternal High-Fat Diet Promotes the Development and Progression of Prostate Cancer in Transgenic Adenocarcinoma Mouse Prostate Offspring

Yang

et al. 2018

Cell Physiol Biochem

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Background/Aims: We aim to investigate the impact of maternal high fat diet (HFD) on the development and progression of prostate cancer (PCa) in transgenic adenocarcinoma mouse prostate (TRAMP) offspring. Methods: The TRAMP model was used, and divided into maternal HFD group and normal diet (ND) group in the present study. Each group contained 36 TRAMP mice. Serum levels of leptin, adiponectin, interleukin (IL) -1α, IL-1β, IL-6, tumor necrosis factor-α and monocyte chemotactic protein-1 were measured by the 20th, 24th and 28th week old through ProcartaPlex Multiplex Immunoassay. Body fat ratio was measured by MiniQMR. Tumor formation rate was measured through hematoxylin and eosin (H&E) staining, and mortality rate was measured meantime. Western blot was applied to determine the levels of Protein Kinase B (Akt) and Phosphatase and tensin homolog (PTEN). Results: The mortality rate of maternal HFD group was significantly higher than that of ND group (P = 0.046). The tumor formation rate was significantly higher in maternal HFD group than in ND group only in 20th week subgroup (P = 0.040). A significant increase of leptin was seen in maternal HFD 20th and 24th week subgroups (P = 0.001 and < 0.001, respectively) and a decrease of adiponectin was seen in maternal HFD 20th and 28th week subgroups (P =0.006 and < 0.001, respectively). Besides, an activated phos-Akt (P-Akt) and deactivated PTEN were observed in maternal HFD group. Conclusions: Maternal HFD could increase the standard serum leptin level, inhibit the expression of PTEN protein, promote P-Akt protein expression, activate the PI3K/Akt pathway, and ultimately promote the development and progression of PCa in TRAMP offspring.

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Adiponectin as a potential tumor suppressor inhibiting epithelial‐to‐mesenchymal transition but frequently silenced in prostate cancer by promoter methylation

Abstract: Our findings indicated that endogenous ADN may function as a tumor suppressor gene through inhibiting EMT of PCa cells but is down-regulated in PCa via promoter hypermethylation.

Cited by 33 publications

References 35 publications

Adiponectin deficiency contributes to the development and progression of benign prostatic hyperplasia in obesity

Adiponectin deficiency contributes to the development and progression of benign prostatic hyperplasia in obesity

Leptin, Adiponectin, and Sam68 in Bone Metastasis from Breast Cancer

Maternal High-Fat Diet Promotes the Development and Progression of Prostate Cancer in Transgenic Adenocarcinoma Mouse Prostate Offspring

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