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    • br Adiponectin in prostate cancer PC was

    2024-03-27


    Adiponectin in prostate cancer PC was documented as the leading type of malignancy in males in the US with respect to both the estimated number of cases (22,800) and deaths (27,540) (Siegel et al., 2016). Studies have reported an association between low APN levels and the progression of PC (Michalakis et al., 2015) (Table 2). With increasing age, the prostate gland in men can become enlarged due to testosterone imbalance (Dasgupta et al., 2012). Benign prostatic hyperplasia (BPH) arises when there is abnormal growth of prostate PTC-209 within the gland leading to disruption of apoptosis (Gleason, 1992). During prostate carcinogenesis, normal prostate cells begin to develop an unusual appearance and are known as prostatic intraepithelial neoplasia (PIN), which is usually characterized into two different types: high grade PIN and low grade PIN (Bostwick, 1995). Low grade PIN is not greatly altered from normal tissue, however, high grade PIN is believed to be abnormal and associated with PC development (Bostwick, 1995). More specifically, the cellular components including the nucleus appear abnormal and this eventually leads to aggressive proliferation, causing a disruption in the cycle of an uninterrupted turnover of cells within the prostate gland (Gleason, 1992). This can finally lead to the formation a locally intrusive tumor which can later become metastatic (Koochekpour, 2011). This series of events is critical in PC progression. An investigative study was performed by Di Sebastiano et al. (2016) in order to illustrate the effects of lifestyle factors such as diet and exercise as well as metabolic perturbations on the prognosis of prostate cancer treatments. In this study, 51 men were evaluated and their results were compared to their biopsy results. It was observed that a number of factors related to obesity were linked to highly aggressive prostate cancer prognosis (Di Sebastiano et al., 2016). A contrasting study was performed by Tan et al. (Tan et al., 2015), which suggests APN as a tumor suppressing agent in prostate cancer. This study was performed using 96 PCa patients and 15 patients with Benign Prostatic Hyperplasia (BPH) (Table 2). It was observed that APN inhibits proliferation and invasion in prostate cancer. Whereas, knockdown of APN increases proliferation, invasion, EMT (Epithelial-to-mesenchymal Transition) process, methylation and decreases tumor suppressing genes. These effects were reserved upon treatment with 5-aza and TSA (Tan et al., 2015). Therefore, these findings suggest that APN acts as a tumor suppressor through inhibiting EMT but is down-regulated by DNA methylation. Another study conducted by Urushima et al. (2015) investigated the effect of Androgen deprivation therapy (ADT) on APN and serum aP2 levels in prostate cancer patients. It was observed that six months after ADT, the APN and serum aP2 levels increased significantly even though there were no changes observed in the body weight of the patients. There was no relation observed between APN levels and serum aP2 (Urushima et al., 2015).
    Adiponectin receptors in prostate cancer development AdipoR1 and R2 showed decreased levels in PC tissues compared to counterpart non-tumorous tissues (Michalakis et al., 2007). This might be due to the molecular connection between obesity and PC along with the interaction of other adipokines and hormones. Another study found that there is a positive relationship between AdipoR2 and PC development (Rider et al., 2015). This accumulating evidence on the expression of three APN receptors, especially AadipoR2, and their functionality in PC development is an exciting area of research.
    Obesity, adiponectin and prostate cancer In males, obesity (BMI of 30kg/m2 or more), is known to increase the chance of getting PC (Gbenou, 2013). Lu et al. (2012) suggested that obesity may induced the PC due to low levels of circulatory APN causing in high oxidative stress. Several evidences to support a relationship between obesity, low circulatory APN leading to an increased inflammation, and more chance getting PC (Nock and Berger, 2010, Goktas et al., 2005) (Table 2). Low APN receptor expression within the body leads to deregulation of signaling pathways such as AMPK and mTOR signaling, which has notable function in the carcinogenesis of cancers including prostate, melanoma, and glioblastoma (Obeid and Hebbard, 2012, Otvos et al., 2011). Together, these factors significantly contribute to the development of PC.